Affinage

CD22

B-cell receptor CD22 · UniProt P20273

Length
847 aa
Mass
95.3 kDa
Annotated
2026-06-09
100 papers in source corpus 32 papers cited in narrative 32 extracted findings
Cross-family judge vs UniProt: Affinage preferred faithfulness: 8/8 claims corpus-supported (100%)

Mechanistic narrative

Synthesis pass · prose summary of the discoveries below

CD22 (Siglec-2) is a B cell-restricted inhibitory co-receptor that sets the threshold for B cell antigen receptor (BCR) signaling by recognizing α2,6-linked sialic acid glycans through its N-terminal lectin domain (PMID:8463234, PMID:28970495). It associates with the BCR complex across multiple immunoglobulin isotypes and becomes rapidly tyrosine-phosphorylated by Lyn and Syk within a minute of receptor crosslinking (PMID:8475064, PMID:7684686, PMID:11551923). Phosphorylation of its cytoplasmic ITIM tyrosines recruits and activates the phosphatase SHP-1, which dephosphorylates BCR signaling components and raises the activation threshold, while a separate tyrosine (Tyr-828/Y807) recruits Grb2 (PMID:7618087, PMID:8627166, PMID:11551923). Through this SHP-1 axis CD22 attenuates downstream Vav phosphorylation and dampens calcium signaling, in part by activation-dependent association with and potentiation of the plasma membrane calcium-ATPase (PMCA) to enhance Ca2+ efflux (PMID:9371816, PMID:15133509). CD22-deficient mice exhibit heightened Ca2+ flux, increased BCR-induced apoptosis, shortened B cell lifespan, and impaired T-independent responses, establishing its role as a negative regulator of B cell activation in vivo (PMID:9016707, PMID:23836650). CD22's ligand-binding and signaling domains act reciprocally: cis engagement by α2,6-sialylated ligands (including CD45, IgM, and the preferred 6-sulfo-LacNAc determinant) organizes CD22 into mobile nanodomains controlling its proximity to the BCR, whereas trans engagement by sialylated multivalent antigens or soluble IgM strongly inhibits BCR signaling (PMID:16369536, PMID:23836650, PMID:19202057, PMID:26671981, PMID:21956693, PMID:17728258, PMID:29146181). CD22 also directs its own clathrin-mediated endocytosis via tyrosine-based motifs that bind the AP-2 adaptor subunit AP50 (PMID:7722303, PMID:12646615). Beyond B cells, CD22 negatively regulates TLR signaling through induction of SOCS1/3 (PMID:21178327), controls B cell mucosal homing via a CD22-SHP1-integrin β7 axis (PMID:33589816), and acts as a negative regulator of microglial phagocytosis in the aged brain whose blockade restores homeostatic function, with soluble CD22 engaging IGF2R to disrupt lysosomal trafficking (PMID:30944478, PMID:34851695).

Mechanistic history

Synthesis pass · year-by-year structured walk · 29 steps
  1. 1990 Medium

    Established CD22 as an Ig-superfamily adhesion molecule before its signaling role was known, placing it structurally among MAG-related proteins.

    Evidence Cell adhesion assay with CD22-transfected cells and structural homology analysis

    PMID:1691828

    Open questions at the time
    • Did not identify the molecular nature of the adhesion ligand
    • No link to signaling function
  2. 1993 High

    Defined the molecular basis of CD22 ligand recognition as a sialic acid-binding lectin specific for α2,6-linked sialic acids, identifying CD45 as the first ligand.

    Evidence Soluble CD22-Ig fusion binding assays, sialyltransferase transfection, and periodate oxidation

    PMID:8463234

    Open questions at the time
    • Did not resolve cis versus trans ligand biology
    • Endogenous physiological ligands not yet defined
  3. 1993 High

    Showed CD22 physically associates with the BCR complex and is rapidly tyrosine-phosphorylated on receptor crosslinking, linking it to BCR signaling.

    Evidence Co-immunoprecipitation with Igα/Igβ in digitonin and in vitro kinase assays across multiple BCR isotypes

    PMID:7684686 PMID:8475064

    Open questions at the time
    • Low stoichiometry of association left functional consequence unclear
    • Kinases responsible not yet identified
  4. 1995 High

    Identified SHP-1 as the effector recruited by phospho-CD22 and demonstrated functionally that CD22 raises the BCR activation threshold ~100-fold, defining it as an inhibitory switch.

    Evidence Co-IP of phospho-CD22 with SHP and B cell activation threshold assays

    PMID:7618087

    Open questions at the time
    • Specific ITIM residues mediating recruitment not yet mapped
    • Downstream substrates of SHP-1 not delineated
  5. 1996 High

    Resolved the inhibitory complex architecture, showing SHP-1 binds CD22 via its N-terminal SH2 domain within CD22/SHP-1/Syk/PLCγ1 assemblies and dephosphorylates CD22.

    Evidence Co-IP of multiprotein complex, SH2 domain mapping, and COS-cell reconstitution with catalytically inactive PTP-1C

    PMID:8627166

    Open questions at the time
    • In vivo significance of complex not established at this stage
  6. 1995 High

    Showed CD22 is constitutively endocytosed and degraded in an acidic compartment, establishing trafficking behavior independent of BCR or CD19 signaling.

    Evidence Flow cytometry and neuraminidase shift/protection assays under multiple stimulation conditions

    PMID:7722303

    Open questions at the time
    • Endocytic machinery not identified
    • Functional role of constitutive turnover unclear
  7. 1997 High

    Genetic knockout established CD22 as a bona fide negative regulator of BCR signaling in vivo, with effects on Ca2+ flux, apoptosis, B cell lifespan, and immune responses.

    Evidence CD22-deficient mice with Ca2+ flux, proliferation, and immune response assays

    PMID:9016707

    Open questions at the time
    • Molecular pathway linking CD22 loss to phenotypes not fully resolved
  8. 1997 High

    Identified Vav as a regulated node and revealed reciprocal CD19 (positive) / CD22 (negative) control of BCR signaling thresholds.

    Evidence Phospho-Vav immunoblotting in CD22- and CD19-deficient mouse B cells under BCR/CD19 crosslinking

    PMID:9371816

    Open questions at the time
    • Mechanism connecting SHP-1 to Vav not directly demonstrated
  9. 1999 Medium

    Connected CD22 to apoptotic outcome by showing CD22 ligation activates SAPK/JNK and downregulates Bcl-xL/Mcl-1, distinct from BCR-driven ERK activation.

    Evidence Kinase activity assays, AP-1 EMSA, and Bcl-2 family Western blots in primary and lymphoma B cells

    PMID:10438726

    Open questions at the time
    • Single-lab pathway analysis without genetic confirmation
    • Relevance to physiological CD22 ligation unclear
  10. 1999 High

    Placed CD45 upstream of CD22 phosphorylation, showing CD45 sequestration enhances CD22 phosphorylation and SHP-1 recruitment to restrain Ca2+ signaling.

    Evidence CD45-deficient B cells, CD45 capping, SHP-1 co-IP, and dominant-negative SHP-1 rescue of Ca2+ flux

    PMID:10228003

    Open questions at the time
    • Whether CD45 acts via lectin-glycan or phosphatase activity not fully separated
  11. 2001 High

    Mapped distinct cytoplasmic modules — ITIM tyrosines for SHP-1 versus Tyr-828 for Grb2 — and assigned Lyn and Syk as the kinases driving CD22 phosphorylation.

    Evidence Systematic tyrosine mutagenesis, SHP-1/Grb2 co-IP, and PP1 inhibitor in kinase-deficient cells

    PMID:11551923

    Open questions at the time
    • Functional role of Grb2 recruitment to CD22 not resolved
  12. 2003 High

    Identified AP50/AP-2 binding to CD22 tyrosine-based motifs as the basis for clathrin-mediated endocytosis, explaining the earlier observed constitutive internalization.

    Evidence Yeast two-hybrid, α-adaptin co-precipitation with CD22 mutants, and internalization assays in Jurkat transfectants

    PMID:12646615

    Open questions at the time
    • Interplay between AP-2 endocytic motif (Tyr-843) and ITIM signaling not fully separated
  13. 2004 High

    Revealed a non-SHP-1 mechanism of Ca2+ control: CD22 associates with and potentiates PMCA in an activation- and tyrosine-dependent manner to enhance Ca2+ efflux.

    Evidence PMCA/CD22 co-IP, CD22 tyrosine mutants, and PMCA4 knockout with Ca2+ flux assays

    PMID:15133509

    Open questions at the time
    • Direct versus SHP-1-bridged nature of CD22-PMCA association not fully resolved
  14. 2005 High

    Used genetic epistasis to prove that suppressed BCR signaling in ST6Gal-I-deficient B cells is mediated through CD22 and linked ligand loss to BCR redistribution into clathrin-rich microdomains.

    Evidence Cd22-/- St6gal1-/- double knockout mice, Ca2+ flux, and membrane microdomain analysis

    PMID:16369536

    Open questions at the time
    • Mechanism of ligand-controlled CD22-BCR positioning not yet at molecular resolution
  15. 2006 High

    Showed that loss of α2,6-sialic acid ligands drives constitutive IgM endocytosis and Lyn-independent SHP-1 recruitment to CD22, all reversed by CD22 co-deficiency.

    Evidence ST6Gal-I/CD22 double knockouts, receptor half-life and endocytosis assays, SHP-1 co-IP, Lyn inhibition

    PMID:16782884

    Open questions at the time
    • Lyn-independent phosphorylation mechanism left unexplained
  16. 2006 Medium

    Demonstrated heterogeneous, stimulus-dependent phosphorylation of CD22 tyrosines, with Y762 fastest and CD40 selectively boosting ITIM phosphorylation.

    Evidence Site-specific phospho-antibodies to four CD22 motifs with anti-IgM and anti-CD40 stimulation

    PMID:16393971

    Open questions at the time
    • Single-lab phospho-antibody data
    • Functional consequence of differential site phosphorylation not tested
  17. 2007 Medium

    Defined the preferred human endogenous CD22 ligand as α2,6-sialylated 6-sulfo-LacNAc, adding sulfation as a recognition determinant.

    Evidence Sulfation inhibition (NaClO3) and blocking mAb in B cell-CD22 binding assays

    PMID:17728258

    Open questions at the time
    • Single-lab biochemical study
    • In vivo requirement for sulfation not tested genetically
  18. 2008 Medium

    Identified a non-sialylated, DC-associated CD22 ligand that mediates contact-dependent inhibition of B cell proliferation by immature dendritic cells.

    Evidence DC-B cell co-culture, CD22 and ST6Gal-I knockouts, neuraminidase/periodate resistance controls

    PMID:18354178

    Open questions at the time
    • Molecular identity of the second ligand unknown
    • Single-lab finding
  19. 2009 Medium

    Showed that trans engagement of CD22 by sialylated multivalent antigens is itself sufficient to suppress BCR signaling and B cell activation.

    Evidence Synthetic sialylated multivalent antigens with Ca2+ flux and activation assays

    PMID:19202057

    Open questions at the time
    • Single-lab finding using synthetic ligands
    • Physiological source of trans ligands not addressed here
  20. 2011 Medium

    Identified soluble IgM as a natural α2,6-sialylated trans ligand activating CD22, implicating a negative feedback loop on B cell activation.

    Evidence Trans activation assays with sIgM-antigen complexes and Ca2+ signaling readouts

    PMID:21956693

    Open questions at the time
    • In vivo contribution of sIgM-CD22 feedback not established
  21. 2010 High

    Extended CD22's inhibitory role beyond the BCR by showing it negatively regulates TLR3/4/9 signaling via SOCS1/3 induction.

    Evidence CD22 knockout mice, ectopic CD22 rescue, TLR ligand proliferation assays, and TLR4-NF-κB reporter

    PMID:21178327

    Open questions at the time
    • Mechanistic link between CD22 and SOCS induction not resolved
  22. 2013 High

    Established that the ligand-binding and ITIM signaling domains of CD22 reciprocally regulate BCR Ca2+ signaling using domain-specific knockin mice.

    Evidence Knockin mice with mutated ligand-binding domain or ITIM motifs, Ca2+ flux and survival assays

    PMID:23836650

    Open questions at the time
    • Spatial mechanism by which cis ligand controls CD22-BCR association not directly imaged here
  23. 2015 High

    Revealed that CD22 organizes into highly mobile nanodomains whose fast diffusion, dependent on CD45 and the lectin domain, enables 'global BCR surveillance' in cooperation with the cortical cytoskeleton.

    Evidence Super-resolution microscopy, single-particle tracking, Brownian dynamics simulation, and lectin/CD45 mutants

    PMID:26671981

    Open questions at the time
    • Molecular bridge between CD22 and the cortical cytoskeleton not identified
  24. 2017 High

    Solved the CD22 ectodomain crystal structure, attributing α2,6-sialic acid specificity to a pre-formed β-hairpin and an extended conformation favoring nanocluster formation and trans binding, plus defining the epratuzumab epitope.

    Evidence X-ray crystallography at 2.1 Å and 3.1 Å with glycosylation site mapping

    PMID:28970495

    Open questions at the time
    • Structure of full-length receptor and cytoplasmic signaling module not determined
  25. 2017 Medium

    Used in situ proximity labeling to define CD22 cis-ligands (CD45, IgM) as α2,6-sialic acid-dependent partners that are already pre-positioned near CD22.

    Evidence Biotin-tyramide proximity labeling on living B cells with ST6GalI-/- and Cmah-/- controls and mass spectrometry

    PMID:29146181

    Open questions at the time
    • Single-lab method
    • Functional consequence of each cis interaction not dissected
  26. 2021 High

    Defined a CD22-SHP1-integrin β7 axis in which sialic acid-dependent CD22-β7 association restrains β7 endocytosis to enhance α4β7 display and mucosal B cell homing.

    Evidence Domain-specific knockin/knockout mice, CD22-β7 co-IP, surface α4β7 flow cytometry, and GALT homing assays

    PMID:33589816

    Open questions at the time
    • Whether this axis operates in human mucosal immunity not addressed
  27. 2019 High

    Identified CD22 as a negative regulator of microglial phagocytosis upregulated in the aged brain, with blockade restoring clearance of myelin, amyloid-β, and α-synuclein and improving cognition.

    Evidence CRISPR-Cas9 knockout screen, RNA-seq, in vivo CD22-blocking antibody, phagocytosis and cognitive assays

    PMID:30944478

    Open questions at the time
    • Intracellular signaling mediating anti-phagocytic effect in microglia not fully defined here
  28. 2021 High

    Identified IGF2R as a receptor for soluble CD22 in myeloid cells, with sCD22 docking near mannose-6-phosphate-binding domains to disrupt lysosomal trafficking, linking CD22 to lysosomal dysfunction.

    Evidence Unbiased genetic and proteomic screens, IGF2R truncation, and lysosomal trafficking assays in NPC1 iPSC-microglia with CD22 blockade

    PMID:34851695

    Open questions at the time
    • How sCD22 is generated in vivo not established
    • Relationship to membrane CD22 anti-phagocytic function unresolved
  29. 2023 Medium

    Placed CD22 downstream of Notch1 in regulatory T cells, where it destabilizes Tregs via mTORC1 and promotes inflammation, with relevance to MIS-C patient variants.

    Evidence Patient NUMB/NUMBL variant analysis, Notch1 perturbation, CD22 expression and mTORC1 assays, Treg stability assays

    PMID:36282598

    Open questions at the time
    • Single study
    • Mechanism by which CD22 engages mTORC1 in Tregs not resolved

Open questions

Synthesis pass · forward-looking unresolved questions
  • How CD22's biochemically defined inhibitory signaling modules are mechanistically repurposed across distinct cell types — B cell, microglial, and Treg contexts — and whether common downstream effectors unify these roles remains unresolved.
  • No unifying signaling model linking BCR, TLR, phagocytic, and Treg functions
  • Mechanism connecting CD22 to SOCS and mTORC1 not defined
  • Generation and physiological role of soluble CD22 unclear

Mechanism profile

Synthesis pass · controlled-vocabulary classification · explore literature graph →
Molecular activity
GO:0060089 molecular transducer activity 4 GO:0098631 cell adhesion mediator activity 4 GO:0060090 molecular adaptor activity 3 GO:0098772 molecular function regulator activity 3 GO:0038024 cargo receptor activity 2
Localization
GO:0005886 plasma membrane 4 GO:0005764 lysosome 2 GO:0031410 cytoplasmic vesicle 2
Pathway
R-HSA-162582 Signal Transduction 5 R-HSA-168256 Immune System 4 R-HSA-5653656 Vesicle-mediated transport 2
Partners
AP50 (AP2M1)CD45GRB2ITGB7LYNPMCA (ATP2B4)SHP-1 (PTPN6)SYK
Complex memberships
BCR complexCD22/SHP-1/Syk/PLCγ1 inhibitory complex

Evidence

Reading pass · 32 per-paper findings extracted from the source corpus
Year Finding Method Journal Conf PMIDs
1993 CD22 is a sialic acid-binding lectin that recognizes α2,6-linked sialic acids on ligands; a soluble CD22-Ig fusion protein binds to sialoglycoproteins in an α2,6-linkage-dependent manner, and truncation of sialic acid side chains by periodate oxidation abolishes binding. CD45 was identified as the first CD22 ligand. Soluble CD22-Ig fusion protein binding assay, COS cell transfection with α2,6-sialyltransferase, periodate oxidation experiments The Journal of biological chemistry High 8463234
1990 CD22 mediates adhesion of monocytes and erythrocytes to B cells; CD22 shares structural homology with myelin-associated glycoprotein (MAG), placing it in the Ig superfamily as an adhesion molecule. Cell adhesion assay with CD22-transfected cells, structural analysis Nature Medium 1691828
1993 CD22 associates with the surface IgM-B cell antigen receptor (BCR) complex; CD22 is co-immunoprecipitated with the sIgM-BCR complex components (Igα/mb-1, Igβ/B29) maintained in digitonin, and CD22 undergoes rapid and striking tyrosine phosphorylation after sIgM crosslinking. CD22 contains the ARHI motif present in antigen receptor molecules. Co-immunoprecipitation in digitonin, in vitro kinase assay, immunoblot with anti-CD22 antiserum Proceedings of the National Academy of Sciences of the United States of America High 8475064
1993 CD22 associates with the B cell antigen receptor (BCR) across multiple isotypes (IgM, IgD, IgG) in both Burkitt lymphoma lines and tonsil cells; the association is specific and stable but of low stoichiometry (0.2–2% of membrane immunoglobulin). CD22 becomes tyrosine phosphorylated within one minute after antigen-receptor cross-linking. In vitro kinase assay, Western blotting, co-immunoprecipitation with multiple BCR isotypes and cell types European journal of immunology High 7684686
1995 Tyrosine-phosphorylated CD22 binds and activates SHP (SHP-1), a protein tyrosine phosphatase that negatively regulates BCR signaling. Ligation of CD22 to prevent its co-aggregation with mIg lowers the threshold for mIg-mediated B cell activation by a factor of 100, establishing CD22 as a molecular switch for SHP. Co-immunoprecipitation of phospho-CD22 with SHP, B cell activation threshold assay, CD22 ligation experiments Science (New York, N.Y.) High 7618087
1996 BCR cross-linking causes PTP-1C (SHP-1) to translocate from cytosol to particulate fraction and associate with tyrosyl-phosphorylated CD22 (140–150 kDa). The association is mediated by the N-terminal SH2 domain of PTP-1C. CD22/PTP-1C/Syk/PLCγ1 complexes can be isolated from stimulated B cells. Binding of PLCγ1 and Syk to CD22 is mediated by the N-terminal SH2 domain of PLCγ1 and C-terminal SH2 domain of Syk respectively. In COS cells, wild-type PTP-1C dephosphorylates CD22, whereas null-mutant PTP-1C (PTP-1CM) does not. Co-immunoprecipitation, Western blotting, COS cell transfection with wild-type and catalytically inactive PTP-1C, SH2 domain binding analysis The Journal of experimental medicine High 8627166
1997 CD22-deficient mice generated by targeted gene inactivation show normal B cell development but increased Ca2+ influx and increased apoptosis after BCR crosslinking in vitro, increased proliferative response to LPS, shorter B cell lifespan in vivo, impaired T-cell-independent immune responses, and absence of recirculating B cells from bone marrow. This establishes CD22 as a negative regulator of BCR signaling in vivo. Targeted gene inactivation (knockout mice), flow cytometry, Ca2+ flux assay, proliferation assays, immune response assays Current biology : CB High 9016707
1995 CD22 is constitutively endocytosed by unstimulated B cell lines and subsequently degraded in an acidic intracellular compartment (presumably lysosomes) without detectable recycling to the cell surface. Ligation of CD22 with anti-CD22 mAbs markedly increases internalization but does not affect degradation rate. Internalization is not affected by phorbol ester or ligation of CD19 or sIgM. Flow cytometry, neuraminidase protection and neuraminidase shift assays, stimulation with phorbol esters and mAbs Journal of immunology (Baltimore, Md. : 1950) High 7722303
1997 CD22 negatively regulates Vav tyrosine phosphorylation downstream of BCR crosslinking; in CD22-deficient B cells, Vav phosphorylation is uniquely augmented after BCR or CD19 crosslinking. Simultaneous crosslinking of CD19 with the BCR substantially decreases Vav phosphorylation when CD22 is expressed, revealing reciprocal regulation of BCR signaling thresholds by CD19 (positive) and CD22 (negative) via Vav. Immunoprecipitation and Western blot for phospho-Vav in CD22-deficient and CD19-deficient mice B cells, BCR and CD19 crosslinking Proceedings of the National Academy of Sciences of the United States of America High 9371816
2001 CD22 cytoplasmic domain contains two functionally distinct domains: (1) two C-terminal ITIM tyrosines (Tyr-843 and Tyr-863) required for efficient SHP-1 recruitment after BCR ligation, and (2) a separate tyrosine (Tyr-828) required for inducible Grb2 recruitment. Both Lyn and Syk are individually required for maximal CD22 tyrosine phosphorylation; together they account for all constitutive and induced phosphorylation. Mutagenesis of CD22 cytoplasmic tyrosines, co-immunoprecipitation of SHP-1 and Grb2, use of Src kinase inhibitor PP1, kinase-deficient cell experiments The Journal of biological chemistry High 11551923
2004 CD22 attenuates B cell Ca2+ signaling by potentiating plasma membrane calcium-ATPase (PMCA) activity. PMCA co-immunoprecipitates with CD22 in an activation-dependent manner. CD22 cytoplasmic tyrosine residues are required for PMCA association and enhanced Ca2+ efflux. CD22 regulation of Ca2+ efflux and the Ca2+ response also requires SHP-1. Disruption of PMCA4a/4b by homologous recombination attenuates CD22-mediated Ca2+ effects. Co-immunoprecipitation of PMCA with CD22, PMCA inhibition, homologous recombination knockout of PMCA4, CD22 cytoplasmic tyrosine mutants, Ca2+ flux assay Nature immunology High 15133509
2005 Mice deficient in both CD22 and the ST6Gal-I enzyme that synthesizes the CD22 α2,6-sialic acid ligand (Cd22-/- St6gal1-/- double knockouts) show restored BCR signaling compared to St6gal1-/- single knockouts, demonstrating that the suppressed BCR signaling in ligand-deficient B cells is mediated through CD22. B cells lacking ST6Gal-I show a net redistribution of BCR to clathrin-rich microdomains containing most CD22. Double knockout mouse generation, Ca2+ flux assay, confocal microscopy/membrane microdomain fractionation Nature immunology High 16369536
2006 ST6Gal-I deficiency (loss of CD22 α2,6-sialic acid ligands) induces constitutive IgM receptor endocytosis coincident with increased colocalization of BCR with CD22 and constitutive SHP-1 recruitment to CD22 independent of Lyn kinase. Co-deficiency with CD22 restores IgM receptor half-life at the cell surface and reverses membrane trafficking and signaling alterations, establishing a CD22-dependent mechanism. ST6Gal-I and CD22 double knockout mice, antigen receptor half-life and endocytosis assays, SHP-1 co-immunoprecipitation, Lyn kinase inhibitor studies Molecular and cellular biology High 16782884
1992 CD22 directly interacts with multiple isoforms of CD45 including CD45RO on T cells; cross-linking of CD3 and CD22 ligands together (anti-CD3 + soluble CD22) blocks anti-CD3-induced intracellular Ca2+ increase and inhibits tyrosine phosphorylation of PLCγ1 in T cells, indicating CD22 can modulate T cell signaling via CD45 engagement. Direct binding assay of CD22 with CD45 isoforms, Ca2+ flux assay in T cells, tyrosine phosphorylation Western blot Proceedings of the National Academy of Sciences of the United States of America Medium 1438211
1995 CD22-mediated engagement of CD45 on T cells can modulate early T cell signals in antigen receptor/CD3-mediated stimulation. Addition of sialic acid by β-galactoside α-2,6-sialyltransferase to CD22 abrogates CD22-CD45 interactions, establishing that CD22-CD45 binding is sialic acid-dependent. Soluble CD22-Ig fusion protein binding to CD45-chimeric T cells, Ca2+ assay, enzymatic sialylation of CD22 Proceedings of the National Academy of Sciences of the United States of America Medium 7537381
1999 Cross-linking of CD22 on primary B cells activates stress-activated protein kinases (SAPKs/JNKs) but not ERK-2, distinct from BCR ligation which activates ERK-2 without significant SAPK activation. CD22 ligation leads to increased nuclear AP-1 and c-jun levels and downregulation of anti-apoptotic Bcl-xL and Mcl-1, providing a mechanism for CD22-induced apoptosis in Burkitt lymphoma cells. SAPK/JNK and ERK kinase activity assays, nuclear extract AP-1 EMSA, Western blot for Bcl-2 family members, primary B cell and B cell line experiments Blood Medium 10438726
2003 CD22 interacts with AP50, the medium chain subunit of the clathrin adaptor AP-2 complex, via tyrosine-based internalization motifs in its cytoplasmic domain. Tyr-843 is the primary binding site for AP50 with Tyr-863 sufficient for mAb-mediated internalization. This interaction mediates clathrin-dependent endocytosis of CD22. Yeast two-hybrid analysis, co-precipitation of α-adaptin with CD22 mutants, transfectant Jurkat cell internalization assays Journal of immunology (Baltimore, Md. : 1950) High 12646615
2013 CD22 cis-ligand binding domain is crucial for regulating BCR signaling by controlling CD22 association with the BCR. Mice with mutated CD22 ligand-binding domain show strongly reduced Ca2+ signaling. Conversely, mice with mutated CD22 ITIM motifs have increased B cell Ca2+ responses, increased B cell turnover, and impaired B cell survival. Thus the ligand-binding and signaling domains of CD22 reciprocally regulate BCR Ca2+ signaling. Knockin mice with mutated CD22 ligand-binding domain or ITIM motifs, Ca2+ flux assay, B cell survival assays Proceedings of the National Academy of Sciences of the United States of America High 23836650
2009 Sialylated multivalent antigens engage CD22 in trans and inhibit BCR signaling and B cell activation. Exposure of B cells to sialylated antigens inhibits key steps in BCR signaling, revealing that trans interactions (CD22 bound by antigen-displayed sialic acid ligands) are sufficient to suppress B cell activation. Sialylated multivalent antigen synthesis, BCR signaling assays (Ca2+ flux, phosphorylation), B cell activation assays Proceedings of the National Academy of Sciences of the United States of America Medium 19202057
2015 CD22 is organized into highly mobile nanodomains in naïve B cells, as revealed by super-resolution microscopy and single-particle tracking. CD22 lateral diffusion is perturbed in the absence of CD45 or when the CD22 lectin domain is mutated. Brownian dynamic simulations and ex vivo experiments suggest CD22's inhibitory function is enabled by its fast diffusion providing 'global BCR surveillance' at the plasma membrane. The cortical cytoskeleton cooperates with CD22 to restrain BCR signaling. Super-resolution microscopy (STORM/PALM), single-particle tracking, Brownian dynamic simulations, CD22 lectin-domain mutant B cells, CD45-deficient B cells The EMBO journal High 26671981
2017 Crystal structure of human CD22 ectodomain solved at 2.1 Å resolution, revealing that specificity for α2-6 sialic acid ligands is dictated by a pre-formed β-hairpin unique among Siglec family members. The CD22 ectodomain adopts an extended conformation facilitating CD22 nanocluster formation on B cells and trans ligand binding. The structure of CD22 with therapeutic antibody epratuzumab was determined at 3.1 Å, delineating the epratuzumab binding site and revealing a critical role for N-linked glycosylation in antibody engagement. X-ray crystallography (2.1 Å and 3.1 Å structures), structural analysis of ligand-binding β-hairpin, glycosylation site mapping Nature communications High 28970495
2019 CD22 is upregulated on aged microglia and mediates the anti-phagocytic effect of α2,6-linked sialic acid; CD22 was identified as a negative regulator of microglial phagocytosis by CRISPR-Cas9 knockout screens. Inhibition of CD22 promotes clearance of myelin debris, amyloid-β oligomers, and α-synuclein fibrils in vivo. Long-term CNS delivery of a CD22-blocking antibody reprograms microglia toward a homeostatic transcriptional state and improves cognitive function in aged mice. CRISPR-Cas9 knockout screen, RNA sequencing, in vivo antibody blockade, phagocytosis assays, cognitive behavioral testing Nature High 30944478
1999 CD45 regulates tyrosine phosphorylation of CD22 and its association with SHP-1; cross-linking of CD45 induces physical sequestration from CD22, leading to increased CD22 tyrosine phosphorylation and SHP-1 recruitment. In CD45-deficient B cells, CD22 shows increased basal and inducible tyrosine phosphorylation and enhanced SHP-1 recruitment. Expression of catalytically inactive SHP-1 in CD45-deficient cells restored intracellular Ca2+ mobilization. CD45-deficient B cell line, CD45 cross-linking and capping, co-immunoprecipitation of SHP-1 with CD22, expression of catalytically inactive SHP-1, Ca2+ flux assay Journal of immunology (Baltimore, Md. : 1950) High 10228003
2006 CD22 phosphorylation upon BCR ligation is not uniform: Y762 undergoes the most rapid phosphorylation, and ultimately all four tyrosine motifs (Y762, Y807, Y822, Y842) are phosphorylated at ~35% of CD22 molecules. Anti-CD40 stimulation specifically upregulates BCR-induced phosphorylation of ITIM tyrosines Y762 and Y842, but not Y807 (Grb2 site), revealing qualitative differences in CD22 phosphorylation patterns depending on stimulus. Phospho-specific polyclonal antibodies to four CD22 tyrosine motifs, flow cytometry, Western blot, anti-IgM and anti-CD40 stimulation Journal of immunology (Baltimore, Md. : 1950) Medium 16393971
2010 CD22-deficient mice show hyperactivation to TLR3, TLR4, and TLR9 ligands, and this hyperactivation is associated with impaired induction of SOCS1 and SOCS3 (suppressors of cytokine signaling). Antibody-mediated CD22 sequestration on wild-type B cells augments TLR-induced proliferation. Ectopic CD22 expression in CD22-deficient B cell lines blunts TLR responses. CD22 expression in a TLR4 reporter cell line inhibits LPS-induced NF-κB transcription. This establishes CD22 as a negative regulator of TLR signaling in addition to BCR signaling. CD22 knockout mice, TLR ligand stimulation proliferation assays, SOCS1/3 expression analysis, ectopic CD22 expression in knockout B cell line, TLR4-NF-κB reporter assay Journal of innate immunity High 21178327
2011 CD22 serves as a receptor for soluble IgM (sIgM); CD22 is efficiently activated in trans by complexes of antigen and sIgM due to the presence of α2,6-sialic acid glycan ligands on sIgM, establishing sIgM as a natural trans ligand for CD22 and implicating a negative feedback loop for B cell activation analogous to FcγRIIB. Trans activation assay with sIgM-antigen complexes, glycan ligand analysis, Ca2+ signaling readout European journal of immunology Medium 21956693
2008 Immature but not mature dendritic cells (DCs) inhibit BCR-induced B cell proliferation in a contact-dependent manner that requires CD22 but is independent of the ST6Gal-I-generated α2,6-sialic acid CD22 ligand. A second, distinct CD22 ligand is expressed on DCs that is resistant to neuraminidase and sodium metaperiodate, indicating a non-sialylated DC-associated CD22 ligand mediates CD22-dependent DC-B cell inhibitory interaction. Co-culture of bone marrow-derived DCs with B cells, CD22 knockout and ST6Gal-I knockout mice, neuraminidase and periodate treatment, proliferation assays Journal of immunology (Baltimore, Md. : 1950) Medium 18354178
2021 CD22 associates in a sialic acid-dependent manner with integrin β7 on B cell surfaces, and recruits intracellular Shp1 to β7, restraining β7 endocytosis and enhancing surface α4β7 display. B cells lacking CD22, expressing CD22 with mutated Shp1-binding domains, or mutated carbohydrate-binding domains show reduced surface α4β7 and impaired homing to gut-associated lymphoid tissue (GALT). This establishes a CD22-Shp1-integrin β7 axis controlling B cell trafficking in mucosal immunity. CD22 knockout mice, CD22 domain-specific mutant knockin mice, co-immunoprecipitation of CD22 with β7 integrin, flow cytometry of surface α4β7, B cell homing assay to GALT, Shp1-conditional knockout Nature immunology High 33589816
2021 Soluble CD22 (sCD22) binds to insulin-like growth factor 2 receptor (IGF2R) on human myeloid cells as identified by unbiased genetic and proteomic screens. sCD22 docks near mannose 6-phosphate-binding domains of IGF2R and disrupts lysosomal protein trafficking. CD22 blocking antibodies ameliorate lysosome dysfunction in human NPC1 mutant iPSC-derived microglia-like cells. Unbiased genetic screen, proteomic screen, IGF2R targeted truncation, lysosomal trafficking assays in iPSC-derived microglia, CD22 blocking antibody treatment Science translational medicine High 34851695
2023 Notch1 signaling in regulatory T cells (Tregs) induces CD22 expression, which destabilizes Tregs in an mTORC1-dependent manner and promotes systemic inflammation. Dominant-negative mutations in Notch1 regulators NUMB and NUMBL in MIS-C patients lead to Notch1 upregulation and downstream CD22 induction. This Notch1/CD22 signaling axis disrupts Treg function. Genetic analysis of patient variants (NUMB/NUMBL mutations), Notch1 signaling perturbation in Tregs, CD22 expression analysis, mTORC1 pathway assays, functional Treg stability assays The Journal of clinical investigation Medium 36282598
2007 Human B lymphocytes express α2-6-sialylated 6-sulfo-N-acetyllactosamine (6-sulfo-LacNAc) as a preferred endogenous ligand for CD22; NaClO3 inhibition of cellular sulfation and a mAb specific to this determinant almost completely abrogates human B cell binding to CD22, establishing that both α2-6-sialylation and 6-GlcNAc-sulfation are required for optimal CD22 ligand recognition. Sulfation inhibition (NaClO3), blocking mAb to sulfo-LacNAc determinant, B cell-CD22 binding assay The Journal of biological chemistry Medium 17728258
2017 Proximity labeling of CD22 cis-ligands on B cell surface reveals that CD22, CD45, and IgM associate with CD22 through α2,6-sialic acid-dependent lectin-glycan interactions in cis; these molecules are absent from CD22 proximity in ST6GalI-/- B cells lacking α2,6 sialic acids, but are already located at relative proximity through non-lectin-glycan interactions. Biotin-tyramide proximity labeling on living B cells, ST6GalI-/- and Cmah-/- knockout mice, mass spectrometry identification of labeled proteins Biochemical and biophysical research communications Medium 29146181

Source papers

Stage 0 corpus · 100 papers · ranked by NIH iCite citations
Year Title Journal Citations PMID
2021 CAR T cells with dual targeting of CD19 and CD22 in adult patients with recurrent or refractory B cell malignancies: a phase 1 trial. Nature medicine 511 34312556
2012 Anti-CD22-chimeric antigen receptors targeting B-cell precursor acute lymphoblastic leukemia. Blood 490 23243285
1995 A role in B cell activation for CD22 and the protein tyrosine phosphatase SHP. Science (New York, N.Y.) 468 7618087
2019 CD22 blockade restores homeostatic microglial phagocytosis in ageing brains. Nature 369 30944478
1997 CD22 is a negative regulator of B-cell receptor signalling. Current biology : CB 355 9016707
1997 CD22, a B lymphocyte-specific adhesion molecule that regulates antigen receptor signaling. Annual review of immunology 245 9143697
1993 CD22, a B cell-specific immunoglobulin superfamily member, is a sialic acid-binding lectin. The Journal of biological chemistry 200 8463234
2019 CD22 CAR T-cell therapy in refractory or relapsed B acute lymphoblastic leukemia. Leukemia 197 31110217
1990 The B-cell antigen CD22 mediates monocyte and erythrocyte adhesion. Nature 181 1691828
1993 CD22 associates with the human surface IgM-B-cell antigen receptor complex. Proceedings of the National Academy of Sciences of the United States of America 180 8475064
2011 Antibody fusion proteins: anti-CD22 recombinant immunotoxin moxetumomab pasudotox. Clinical cancer research : an official journal of the American Association for Cancer Research 179 22003067
2018 CD22: A Regulator of Innate and Adaptive B Cell Responses and Autoimmunity. Frontiers in immunology 169 30323814
1996 CD22 associates with protein tyrosine phosphatase 1C, Syk, and phospholipase C-gamma(1) upon B cell activation. The Journal of experimental medicine 159 8627166
2021 Antigen-independent activation enhances the efficacy of 4-1BB-costimulated CD22 CAR T cells. Nature medicine 156 33888899
1993 Association of CD22 with the B cell antigen receptor. European journal of immunology 150 7684686
2005 The role of CD22 and other inhibitory co-receptors in B-cell activation. Current opinion in immunology 147 15886119
1991 cDNA cloning of the B cell membrane protein CD22: a mediator of B-B cell interactions. The Journal of experimental medicine 147 1985119
2005 CD22: a multifunctional receptor that regulates B lymphocyte survival and signal transduction. Advances in immunology 145 16227086
2015 Characterization of CD22 expression in acute lymphoblastic leukemia. Pediatric blood & cancer 143 25728039
2017 Molecular basis of human CD22 function and therapeutic targeting. Nature communications 130 28970495
2005 Ablation of CD22 in ligand-deficient mice restores B cell receptor signaling. Nature immunology 128 16369536
2021 Trispecific CD19-CD20-CD22-targeting duoCAR-T cells eliminate antigen-heterogeneous B cell tumors in preclinical models. Science translational medicine 124 33762438
2008 Targeting CD22 reprograms B-cells and reverses autoimmune diabetes. Diabetes 123 18689692
2009 CD22 and Siglec-G: B-cell inhibitory receptors with distinct functions. Immunological reviews 120 19594633
2007 CD22: an inhibitory enigma. Immunology 114 18067554
2021 Combination of CD19 and CD22 CAR-T cell therapy in relapsed B-cell acute lymphoblastic leukemia after allogeneic transplantation. American journal of hematology 110 33725422
2010 CD22 x Siglec-G double-deficient mice have massively increased B1 cell numbers and develop systemic autoimmunity. Journal of immunology (Baltimore, Md. : 1950) 109 20200274
2009 Sialylated multivalent antigens engage CD22 in trans and inhibit B cell activation. Proceedings of the National Academy of Sciences of the United States of America 109 19202057
2007 IgG1 B cell receptor signaling is inhibited by CD22 and promotes the development of B cells whose survival is less dependent on Ig alpha/beta. The Journal of experimental medicine 109 17420268
1992 CD22-mediated stimulation of T cells regulates T-cell receptor/CD3-induced signaling. Proceedings of the National Academy of Sciences of the United States of America 103 1438211
2014 The role of CD22 and Siglec-G in B-cell tolerance and autoimmune disease. Nature reviews. Rheumatology 98 24763061
1995 Constitutive endocytosis and degradation of CD22 by human B cells. Journal of immunology (Baltimore, Md. : 1950) 97 7722303
1995 Construction and characterization of a humanized, internalizing, B-cell (CD22)-specific, leukemia/lymphoma antibody, LL2. Molecular immunology 95 8643111
2013 CD22 ligand-binding and signaling domains reciprocally regulate B-cell Ca2+ signaling. Proceedings of the National Academy of Sciences of the United States of America 91 23836650
2015 Nanoscale organization and dynamics of the siglec CD22 cooperate with the cytoskeleton in restraining BCR signalling. The EMBO journal 90 26671981
1997 CD19 and CD22 expression reciprocally regulates tyrosine phosphorylation of Vav protein during B lymphocyte signaling. Proceedings of the National Academy of Sciences of the United States of America 87 9371816
1995 Regulation of CD45 engagement by the B-cell receptor CD22. Proceedings of the National Academy of Sciences of the United States of America 83 7537381
2001 CD22 regulates B cell receptor-mediated signals via two domains that independently recruit Grb2 and SHP-1. The Journal of biological chemistry 82 11551923
2004 CD22 attenuates calcium signaling by potentiating plasma membrane calcium-ATPase activity. Nature immunology 75 15133509
1998 CD22 negatively and positively regulates signal transduction through the B lymphocyte antigen receptor. Seminars in immunology 75 9695185
2007 Preclinical and clinical evaluation of epratuzumab (anti-CD22 IgG) in B-cell malignancies. Oncogene 72 17530024
2013 Copresentation of antigen and ligands of Siglec-G induces B cell tolerance independent of CD22. Journal of immunology (Baltimore, Md. : 1950) 71 23836061
2021 CD22-directed CAR T-cell therapy induces complete remissions in CD19-directed CAR-refractory large B-cell lymphoma. Blood 69 33512414
1999 CD22 cross-linking generates B-cell antigen receptor-independent signals that activate the JNK/SAPK signaling cascade. Blood 69 10438726
2020 Glycoengineering of NK Cells with Glycan Ligands of CD22 and Selectins for B-Cell Lymphoma Therapy. Angewandte Chemie (International ed. in English) 68 33314603
2004 Molecular interactions regulate BCR signal inhibition by CD22 and CD72. Trends in immunology 66 15364057
2006 ST6Gal-I restrains CD22-dependent antigen receptor endocytosis and Shp-1 recruitment in normal and pathogenic immune signaling. Molecular and cellular biology 65 16782884
2001 CD19, CD21, and CD22: multifaceted response regulators of B lymphocyte signal transduction. International reviews of immunology 65 11913948
2013 Targeting CD22 in B-cell malignancies: current status and clinical outlook. BioDrugs : clinical immunotherapeutics, biopharmaceuticals and gene therapy 64 23696252
2006 CD22 ligand binding regulates normal and malignant B lymphocyte survival in vivo. Journal of immunology (Baltimore, Md. : 1950) 63 16920943
2017 CD22 Ligands on a Natural N-Glycan Scaffold Efficiently Deliver Toxins to B-Lymphoma Cells. Journal of the American Chemical Society 62 28829594
2007 Human B-lymphocytes express alpha2-6-sialylated 6-sulfo-N-acetyllactosamine serving as a preferred ligand for CD22/Siglec-2. The Journal of biological chemistry 62 17728258
2000 Dysregulated expression of the Cd22 gene as a result of a short interspersed nucleotide element insertion in Cd22a lupus-prone mice. Journal of immunology (Baltimore, Md. : 1950) 61 10975807
2022 A novel CD19/CD22/CD3 trispecific antibody enhances therapeutic efficacy and overcomes immune escape against B-ALL. Blood 60 35981465
2020 CD22 Expression in B-Cell Acute Lymphoblastic Leukemia: Biological Significance and Implications for Inotuzumab Therapy in Adults. Cancers 57 32012891
2010 CD22 regulates adaptive and innate immune responses of B cells. Journal of innate immunity 56 21178327
2014 CD22 and Siglec-G regulate inhibition of B-cell signaling by sialic acid ligand binding and control B-cell tolerance. Glycobiology 55 25002414
2012 CD22 and Siglec-G in B cell function and tolerance. Trends in immunology 55 22677186
2022 CD20+CD22+ADAM28+ B Cells in Tertiary Lymphoid Structures Promote Immunotherapy Response. Frontiers in immunology 54 35634306
2021 CD19/CD22 Chimeric Antigen Receptor T Cell Cocktail Therapy following Autologous Transplantation in Patients with Relapsed/Refractory Aggressive B Cell Lymphomas. Transplantation and cellular therapy 54 34425260
1996 Differential expression of CD22 (Lyb8) on murine B cells. International immunology 54 8757957
2013 CD22 ligation inhibits downstream B cell receptor signaling and Ca(2+) flux upon activation. Arthritis and rheumatism 53 23233360
1988 Expression and structure of CD22 in acute leukemia. Blood 50 3258772
2011 The pan-B cell marker CD22 is expressed on gastrointestinal eosinophils and negatively regulates tissue eosinophilia. Journal of immunology (Baltimore, Md. : 1950) 49 22190185
2003 CD22 as a target of passive immunotherapy. Seminars in oncology 49 12720147
2021 Targeting CD22 for the Treatment of B-Cell Malignancies. ImmunoTargets and therapy 47 34262884
2008 Dendritic cell-dependent inhibition of B cell proliferation requires CD22. Journal of immunology (Baltimore, Md. : 1950) 44 18354178
2018 Inotuzumab ozogamicin: a CD22 mAb-drug conjugate for adult relapsed or refractory B-cell precursor acute lymphoblastic leukemia. Drug design, development and therapy 43 30087554
2012 CD22 and autoimmune disease. International reviews of immunology 42 23083346
2024 CD22 CAR T cells demonstrate high response rates and safety in pediatric and adult B-ALL: Phase 1b results. Leukemia 40 38491306
2003 The B cell coreceptor CD22 associates with AP50, a clathrin-coated pit adapter protein, via tyrosine-dependent interaction. Journal of immunology (Baltimore, Md. : 1950) 39 12646615
2021 A novel and efficient tandem CD19- and CD22-directed CAR for B cell ALL. Molecular therapy : the journal of the American Society of Gene Therapy 38 34478871
2007 B cell signaling and autoimmune diseases: CD19/CD22 loop as a B cell signaling device to regulate the balance of autoimmunity. Journal of dermatological science 38 17223015
2024 Inotuzumab Ozogamicin and Low-Intensity Chemotherapy in Older Patients With Newly Diagnosed CD22+ Philadelphia Chromosome-Negative B-Cell Precursor Acute Lymphoblastic Leukemia. Journal of clinical oncology : official journal of the American Society of Clinical Oncology 37 39418626
2023 CD22 blockade modulates microglia activity to suppress neuroinflammation following intracerebral hemorrhage. Pharmacological research 35 37696483
2021 CD22 Blockage Restores Age-Related Impairments of Microglia Surveillance Capacity. Frontiers in immunology 35 34140954
2021 The CD22-IGF2R interaction is a therapeutic target for microglial lysosome dysfunction in Niemann-Pick type C. Science translational medicine 35 34851695
2011 Targeting B lymphoma with nanoparticles bearing glycan ligands of CD22. Leukemia & lymphoma 35 21756025
2009 Identification and characterization of fully human anti-CD22 monoclonal antibodies. mAbs 34 20065646
2002 Differentially regulated expression and function of CD22 in activated B-1 and B-2 lymphocytes. Journal of immunology (Baltimore, Md. : 1950) 34 12055217
2023 CD22 CAR T-cell associated hematologic toxicities, endothelial activation and relationship to neurotoxicity. Journal for immunotherapy of cancer 33 37295816
2011 CD22 serves as a receptor for soluble IgM. European journal of immunology 33 21956693
2022 CD34+CD19-CD22+ B-cell progenitors may underlie phenotypic escape in patients treated with CD19-directed therapies. Blood 32 35421218
2017 Human CD22 Inhibits Murine B Cell Receptor Activation in a Human CD22 Transgenic Mouse Model. Journal of immunology (Baltimore, Md. : 1950) 32 28972089
2002 Expression and function of CD22, a B-cell restricted molecule. Scandinavian journal of immunology 32 11967115
2002 Specifically targeting the CD22 receptor of human B-cell lymphomas with RNA damaging agents: a new generation of therapeutics. Leukemia & lymphoma 31 12148905
2023 The Notch1/CD22 signaling axis disrupts Treg function in SARS-CoV-2-associated multisystem inflammatory syndrome in children. The Journal of clinical investigation 29 36282598
2023 Dual targeting of CD19 and CD22 against B-ALL using a novel high-sensitivity aCD22 CAR. Molecular therapy : the journal of the American Society of Gene Therapy 29 36945773
2019 Coordinated roles for glycans in regulating the inhibitory function of CD22 on B cells. Biomedical journal 29 31627864
2021 A CD22-Shp1 phosphatase axis controls integrin β7 display and B cell function in mucosal immunity. Nature immunology 28 33589816
2017 Proximity labeling of cis-ligands of CD22/Siglec-2 reveals stepwise α2,6 sialic acid-dependent and -independent interactions. Biochemical and biophysical research communications 28 29146181
2006 B cell antigen receptor and CD40 differentially regulate CD22 tyrosine phosphorylation. Journal of immunology (Baltimore, Md. : 1950) 28 16393971
1999 CD45 regulates tyrosine phosphorylation of CD22 and its association with the protein tyrosine phosphatase SHP-1. Journal of immunology (Baltimore, Md. : 1950) 28 10228003
2021 Upregulation of CD22 by Chidamide promotes CAR T cells functionality. Scientific reports 26 34667217
2012 Targeting of CD22-positive B-cell lymphoma cells by synthetic divalent sialic acid analogues. European journal of immunology 26 22777817
2017 Anti-CD22 and anti-CD79b antibody-drug conjugates preferentially target proliferating B cells. British journal of pharmacology 25 28009435
2023 Targeting CD22 for B-cell hematologic malignancies. Experimental hematology & oncology 24 37821931
2013 CD22 is required for protection against West Nile virus Infection. Journal of virology 23 23302871
2023 Decitabine in combination with fludarabine and cyclophosphamide as a lymphodepletion regimen followed by CD19/CD22 bispecific targeted CAR T-cell therapy significantly improves survival in relapsed/refractory B-ALL patients. Experimental hematology & oncology 20 37038230
2022 Targeting CD22 on memory B cells to induce tolerance to peanut allergens. The Journal of allergy and clinical immunology 20 35839842

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