Affinage

CD79A

B-cell antigen receptor complex-associated protein alpha chain · UniProt P11912

Length
226 aa
Mass
25.0 kDa
Annotated
2026-06-09
100 papers in source corpus 20 papers cited in narrative 20 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

CD79A (Igα/mb-1) is a B-lineage-restricted transmembrane glycoprotein that serves as the signal-transduction component of the B cell antigen receptor (BCR), functioning as the B-cell equivalent of CD3 (PMID:2463161, PMID:7632952). It obligatorily heterodimerizes with CD79B (Igβ), and this heterodimerization is required for maturation of BCR N-glycans, escape from the endoplasmic reticulum, and surface display of IgM; loss of either partner or a heterodimerization-defective CD79B mutant blocks surface BCR expression (PMID:36426942). The Igα cytoplasmic domain is both necessary and sufficient to reconstitute Ca2+ flux and phosphorylation responses when fused to a signaling-deficient IgM, establishing it as a self-contained signaling module (PMID:7688784). CD79A signaling is functionally partitioned: its ITAM tyrosines drive canonical activation, while the non-ITAM tyrosines Y176 and Y204 are phosphorylated upon BCR engagement and recruit BLNK, Vav, and Grb2 to mediate antigen internalization into the MHC class II compartment for presentation to T cells, and additionally support a distinct T-independent activation pathway feeding NF-κB/JNK/ERK signaling and proliferation (PMID:11859098, PMID:16860757). The Igα cytoplasmic domain is dominant over Igβ for BCR internalization and lysosomal trafficking (PMID:20837062). Beyond antigen-driven signaling, ligand-independent tonic signals through the Igα/Igβ cytoplasmic domains drive pre-BCR-dependent processes—proliferation, suppression of VH(D)JH recombination, and induction of kappa light chain expression—and support follicular B cell development (PMID:15240688, PMID:17114463). Consistent with this central role, homozygous loss-of-function mutations in CD79A cause a complete block in B cell development at the pro-B to pre-B transition, producing agammaglobulinemia (PMID:10525050, PMID:11920841). CD79A expression and signaling are further tuned by IL-4, which upregulates Igα/Igβ protein via STAT6 to amplify surface IgM and BCR signaling (PMID:23776171).

Mechanistic history

Synthesis pass · year-by-year structured walk · 14 steps
  1. 1988 High

    Established the molecular identity of CD79A by cloning a B-lineage-restricted surface glycoprotein, defining the entity before any signaling role was known.

    Evidence cDNA cloning, sequence analysis, and surface immunostaining across B and non-B cell lines

    PMID:2463161

    Open questions at the time
    • No functional or signaling role assigned at cloning
    • Partner CD79B and BCR association not yet defined
  2. 1992 Medium

    Resolved the developmental timing of CD79A relative to CD79B, showing the two BCR signaling components are differentially regulated across B cell differentiation.

    Evidence Immunocytochemistry with anti-peptide antibodies on B cell lines, tissues, and leukemias

    PMID:1396979

    Open questions at the time
    • Expression timing does not establish signaling function
    • Single primary method
  3. 1993 High

    Demonstrated that the Igα cytoplasmic domain is necessary and sufficient for BCR signal transduction, defining CD79A as the receptor's signaling module rather than a passive structural subunit.

    Evidence IgM transmembrane mutagenesis and Igα/Igβ cytoplasmic-domain fusion constructs with Ca2+ flux and phosphorylation readouts

    PMID:7688784

    Open questions at the time
    • Downstream effectors of distinct Igα vs Igβ pathways not enumerated
    • In vitro/cell-line context only
  4. 1995 Medium

    Characterized alternatively spliced CD79A transcripts encoding truncated proteins, including a variant lacking extracellular disulfide cysteines that does not support BCR surface expression and is induced by B cell activation.

    Evidence RNase protection, cDNA cloning, transfection reconstitution, and anti-IgM/LPS/IL-4 activation assays

    PMID:7643857 PMID:8747711

    Open questions at the time
    • Physiological role of activation-induced variant unresolved
    • Whether variant acts as a dominant-negative not tested
  5. 1999 High

    Identified CD79A as genetically required for the pro-B to pre-B checkpoint in humans, linking the BCR signaling module to a defined developmental block and to agammaglobulinemia.

    Evidence Genetic screening, B cell developmental immunofluorescence, and V-DJ sequencing in agammaglobulinemia patients, replicated in a second patient

    PMID:10525050 PMID:11920841

    Open questions at the time
    • Molecular signal that arrests development not defined
    • Epistasis only relative to mu-heavy-chain deficiency
  6. 2002 Medium

    Confirmed CD79A loss-of-function as a recurrent cause of agammaglobulinemia in an independent patient, solidifying genotype-phenotype causality.

    Evidence Genetic sequencing and clinical immunological evaluation

    PMID:11920841

    Open questions at the time
    • Single method
    • No functional reconstitution of the specific splice mutation
  7. 2002 High

    Defined the non-ITAM tyrosines Y176/Y204 as the adaptor-recruitment platform that routes the BCR for antigen presentation, separating presentation from canonical activation.

    Evidence Site-directed mutagenesis of Y176/Y204, BLNK reconstitution, antigen presentation and subcellular trafficking assays

    PMID:11859098

    Open questions at the time
    • Relative contribution of Vav vs Grb2 not dissected
    • Structural basis of phospho-tyrosine recognition not resolved
  8. 2004 High

    Showed that ligand-independent tonic signals from the Igα/Igβ cytoplasmic domains alone are sufficient for pre-BCR functions, establishing that receptor aggregation is dispensable for these outputs.

    Evidence Membrane-targeted surrogate Igα/Igβ receptor in primary pro-B cells with proliferation, VDJ recombination, and kappa expression readouts; chicken chimeric CD8α-Igα reconstitution

    PMID:14962183 PMID:15240688

    Open questions at the time
    • Source of tonic signal initiation unknown
    • Igα and Igβ shown to have opposing effects on development in avian model, mechanism unresolved
  9. 2006 High

    Assigned distinct in vivo functions to Igα tyrosine motifs—Y204 to T-independent activation and the ITAM/cytoplasmic domain to follicular B cell development—demonstrating signal partitioning within a single chain.

    Evidence Y204F knock-in mice and chimeric ITAM Tyr→Phe constructs with activation, proliferation, Ca2+, kinase, and B cell subset analyses

    PMID:16860757 PMID:17114463

    Open questions at the time
    • Why marginal zone and B1 subsets fail to form under tonic signaling not explained
    • Direct binding partners of Y204 not all defined
  10. 2007 Medium

    Linked CD79A/CD79B to MHC class II signaling, showing Igα/Igβ co-associate with MHC II to mediate calcium responses.

    Evidence MHC II alpha-chain connecting-peptide mutagenesis, co-IP with Igα/Igβ, and Igβ shRNA knockdown with Ca2+ and cell-death readouts

    PMID:18194817

    Open questions at the time
    • Direct vs indirect association of CD79A specifically not isolated from Igβ
    • Physiological role of MHC II–BCR module unclear
  11. 2010 High

    Mapped the BCR internalization signal to the Igα cytoplasmic domain, showing it is dominant over Igβ for endocytosis and lysosomal trafficking.

    Evidence Igα/Igβ mutant expression in deficient murine lymphoid cells with internalization and subcellular localization assays

    PMID:20837062

    Open questions at the time
    • Endocytic adaptors engaged by the internalization motif not identified
    • Cell-line context only
  12. 2013 Medium

    Established post-translational control of CD79A by IL-4/STAT6 and uncovered an unexpected non-B-cell role on myeloid-derived suppressor cells.

    Evidence IL-4 treatment with STAT6 dependence, co-IP and signaling assays in primary B cells; CD79A crosslinking with Syk/BLNK/ERK/STAT3 readouts and tumor assays on MDSCs

    PMID:23776171 PMID:24146823

    Open questions at the time
    • Mechanism of CD79A surface display on myeloid cells without a conventional BCR unknown
    • Myeloid finding from single lab
  13. 2022 High

    Defined the chaperone mechanism: CD79A/CD79B heterodimerization is required for N-glycan maturation and ER export of the BCR, explaining why either subunit's loss abolishes surface IgM.

    Evidence CRISPR/Cas9 knockout in B lymphoma lines with WT vs heterodimerization-defective CD79B G137S rescue, N-glycan maturation and surface IgM analyses

    PMID:36426942

    Open questions at the time
    • Step at which immature BCR is retained in ER not resolved at structural level
    • Whether human developmental block reflects same trafficking defect not directly tested
  14. 2021 Medium

    Demonstrated translational utility of the CD79A signaling domain as a CAR-T co-stimulatory endodomain, leveraging its NF-κB/p38 activation.

    Evidence CD79A/CD40 composite endodomain in CD19 CAR-T cells with signaling, cytotoxicity, and Raji xenograft assays

    PMID:33940156

    Open questions at the time
    • Engineered context does not test endogenous CD79A function
    • Single lab

Open questions

Synthesis pass · forward-looking unresolved questions
  • How CD79A signaling is repurposed on non-B myeloid cells lacking a conventional BCR, and the structural basis for its differential ITAM vs non-ITAM tyrosine partner selection, remain open.
  • No structure of CD79A in complex with downstream adaptors in the corpus
  • Mechanism of CD79A surface expression on myeloid cells unresolved

Mechanism profile

Synthesis pass · controlled-vocabulary classification · explore literature graph →
Molecular activity
GO:0060089 molecular transducer activity 3 GO:0038024 cargo receptor activity 2 GO:0060090 molecular adaptor activity 2 GO:0005198 structural molecule activity 1
Localization
GO:0005886 plasma membrane 3 GO:0005764 lysosome 1 GO:0005783 endoplasmic reticulum 1
Pathway
R-HSA-1266738 Developmental Biology 3 R-HSA-162582 Signal Transduction 3 R-HSA-168256 Immune System 3 R-HSA-392499 Metabolism of proteins 2
Partners
BLNKCD79BGRB2IGMLYNSTAT6SYKVAV
Complex memberships
B cell antigen receptor (BCR) complexCD79A/CD79B heterodimer

Evidence

Reading pass · 20 per-paper findings extracted from the source corpus
Year Finding Method Journal Conf PMIDs
1988 CD79A (mb-1/Ig-alpha) encodes a B-lineage-restricted membrane glycoprotein of 220 amino acids with a leader sequence, extracellular domain with two N-glycosylation sites, transmembrane domain, and cytoplasmic domain; antibodies against the protein stain the surface of pre-B and mature B cell lines but not T cell lines or fibroblasts, establishing it as a B-cell surface protein. cDNA cloning, nucleotide/amino acid sequence analysis, immunostaining with affinity-purified antibodies against fusion protein The EMBO journal High 2463161
1993 Ig-alpha (CD79A) and Ig-beta form the signal-transduction module of the B cell antigen receptor; specific mutations in the IgM transmembrane domain that abrogate Ca2+ flux and phosphorylation responses also uncouple IgM from the Igα/Igβ heterodimer; fusion of the cytoplasmic domain of Igα to signaling-deficient IgM fully reconstitutes Ca2+ flux and phosphorylation, while fusion of Igβ alone restores only Ca2+ responses, demonstrating that Igα and Igβ are both necessary and sufficient for BCR signal transduction and can activate distinct signaling pathways. Mutagenesis of IgM transmembrane domain, cytoplasmic domain fusion constructs, Ca2+ flux assays, phosphorylation assays in B cells The Journal of experimental medicine High 7688784
1992 CD79A (mb-1) protein expression begins earlier than CD79B (B29) in B cell development: mb-1 is expressed in pre-B cells and persists through the plasma cell stage, whereas B29 expression begins later (from the pre-B/cytoplasmic-µ stage) and is absent from plasma cells, establishing differential regulation of the two BCR signaling components during B cell differentiation. Immunocytochemistry with anti-peptide antibodies on B cell lines and lymphoid tissue sections, analysis of acute lymphoblastic leukemia subtypes European journal of immunology Medium 1396979
1995 CD79A (mb-1/CD79a) is physically associated in the B cell membrane with immunoglobulin as part of the CD79 heterodimer (CD79a/CD79b), transmits signal after antigen binding, appears before the pre-B cell stage, and can persist at the plasma cell stage while CD79b is lost; it functions as the B cell equivalent of CD3. Immunohistochemistry with monoclonal antibody JCB117 on 454 paraffin-embedded tissue biopsies covering full range of B cell maturation stages Blood Medium 7632952
1999 Homozygous loss-of-function splice mutation in CD79A (Igalpha) causes a complete block in B cell development at the pro-B to pre-B transition in humans, demonstrating that CD79A is required for progression through this checkpoint; comparison with mu-heavy-chain-deficient patients showed equivalent V-DJ rearrangement diversity, indicating CD79A does not play a critical role before co-expression with mu heavy chain as part of the pre-BCR. Genetic screening, immunofluorescence analysis of B cell developmental stages, V-DJ rearrangement sequencing in an agammaglobulinemia patient The Journal of clinical investigation High 10525050 11920841
2002 Novel homozygous splice mutation (IVS2+1G>A) in CD79A causes B cell-deficient agammaglobulinemia in a second unrelated patient, confirming CD79A mutations as a cause of agammaglobulinemia. Genetic sequencing, clinical immunological evaluation American journal of medical genetics Medium 11920841
2003 CD79A (mb1/Igalpha) undergoes somatic hypermutation (SHM) in germinal center and post-GC B cells, including normal peripheral B cells and malignant B cell lines; mutations are single nucleotide substitutions targeted to SHM hotspots, occurring at frequencies similar to other non-Ig SHM targets but lower than Ig genes, indicating CD79A is a substrate for the SHM machinery. Sequencing of CD79A/mb-1 loci in GC-derived malignant B cell lines and normal peripheral B cells; hotspot analysis Proceedings of the National Academy of Sciences of the United States of America Medium 12651942
1995 Alternative splicing of CD79A (Ig-alpha/mb-1) generates variant transcripts predicted to encode truncated proteins lacking a major portion of the extracellular Ig-like domain; these variants are present in multiple human B cell types detected by RNase protection assay. RNase protection assay, cDNA cloning, sequence analysis of variant transcripts from multiple B cell lines Molecular immunology Medium 7643857
1995 A variant mb-1 transcript produced by alternative splicing encodes a protein that conserves the transmembrane and cytoplasmic portions but lacks extracellular cysteine residues required for disulfide bonds; transfection studies showed this variant mb-1 does not contribute to BCR surface expression; B cell activation (anti-IgM, LPS, or IL-4) induces significant increases in variant transcript levels. Alternative splicing characterization, transfection assays, B cell activation experiments with anti-IgM/LPS/IL-4 Immunology letters Medium 8747711
2002 Receptor-facilitated antigen presentation requires recruitment of the B cell linker protein (BLNK) to CD79A (Igalpha): non-ITAM tyrosines Y176 and Y204 of Igalpha, when mutated, divert BCR complexes to late endosomes but exclude them from vesicle lumena and prevent antigen presentation to T cells; phosphorylation of Y176/Y204 recruits BLNK, Vav, and Grb2; reconstitution with BLNK rescues antigen presentation and entry into the MHC class II compartment. Site-directed mutagenesis of Igalpha non-ITAM tyrosines (Y176/Y204), antigen presentation assays, subcellular trafficking analysis, reconstitution with BLNK Journal of immunology (Baltimore, Md.: 1950) High 11859098
2006 CD79A non-ITAM tyrosine Y204 becomes phosphorylated upon BCR engagement and mediates a distinct T cell-independent B cell activation pathway: knock-in mice with Y204F mutation show selective defects in T-independent B cell activation, proliferation, and antibody responses with reduced BLNK phosphorylation, Ca2+ flux, and NF-κB/JNK/ERK activation, while BCR capping, antigen internalization, antigen presentation, T cell-dependent responses, and Syk phosphorylation remain normal. Targeted knock-in mutagenesis (Y204F) in mice, B cell activation assays, proliferation assays, Ca2+ flux, kinase phosphorylation analysis Immunity High 16860757
2004 Basal (ligand-independent, tonic) signals mediated through CD79A (Igalpha)/Igbeta cytoplasmic domains expressed as a membrane-targeted surrogate receptor in primary pro-B cells are sufficient to drive pre-BCR-dependent processes: enhanced proliferation at low IL-7, suppression of VH(D)JH recombination, and induction of kappa light chain recombination and expression, demonstrating that pre-BCR aggregation is not required for pre-BCR function. Surrogate receptor construct (membrane-targeted Igalpha/Igbeta cytoplasmic domains) introduced into primary pro-B cells by retroviral transduction; proliferation, VDJ recombination, and kappa chain expression assays Journal of immunology (Baltimore, Md.: 1950) High 15240688
2006 CD79A (Igalpha) tonic signaling through its ITAM and cytoplasmic domain supports development of follicular B cells; chimeric protein analysis with Tyr→Phe modifications and single vs. tandem ITAM copies showed both Igalpha and Igbeta support follicular B cell formation under tonic signaling conditions, but neither marginal zone nor B1 B cell subsets develop under purely tonic signal conditions. Chimeric receptor constructs with Tyr→Phe ITAM modifications, gene transfer into RAG2-/- pro-B cell lines and muMT mice, flow cytometric analysis of B cell subsets Journal of immunology (Baltimore, Md.: 1950) High 17114463
2010 The CD79A (Igalpha) cytoplasmic domain is dominant over Igbeta for BCR internalization; the internalization signal is located in a region past the first cytoplasmic tyrosine (Y176); a 4-amino-acid motif within the Igalpha ITAM is sufficient to rescue aberrant internalization; each cytoplasmic domain alone is sufficient for trafficking to lysosomal compartments, but normal trafficking rate requires both Igalpha and Igbeta. Expression of Igalpha/Igbeta mutants in Igalpha/Igbeta-deficient murine lymphoid cell line, internalization assays, subcellular localization analysis Immunology letters High 20837062
2013 IL-4 markedly upregulates Igα (CD79A) and Igβ protein (but not mRNA) expression in primary B cells via STAT6; elevated Igα/Igβ protein forms heterodimers that associate with IgM, promote IgM maturation and surface IgM expression, and result in amplified Lyn-dependent BCR signaling; in vivo pre-germinal center B cells show IL-4-dependent upregulation of Igα, Igβ, and surface IgM with elevated BCR-triggered phospho-ERK. IL-4 treatment of primary B cells, STAT6 requirement analysis, co-immunoprecipitation of heterodimers with IgM, surface IgM flow cytometry, BCR signaling assays, in vivo neutralization of IL-4 Journal of immunology (Baltimore, Md.: 1950) High 23776171
2013 CD79A is unexpectedly expressed on immature bone marrow myeloid cells and is upregulated on myeloid-derived suppressor cells (MDSCs) in mouse models of metastatic cancer; crosslinking CD79A on MDSCs maintained their immature CD11b+Gr1+ phenotype, enhanced migration, increased T cell suppression, and increased pro-tumorigenic cytokine secretion (IL-6, CCL22); CD79A activation on myeloid cells signals through Syk, BLNK, ERK, and STAT3 phosphorylation. CD79A crosslinking with specific antibody on MDSCs, flow cytometry for phenotype, migration assays, T cell suppression assays, cytokine secretion measurement, phosphorylation analysis (Syk/BLNK/ERK/STAT3), in vivo tumor growth assays PloS one Medium 24146823
2022 CRISPR/Cas9 deletion of CD79A (or CD79B) in human B lymphoma cell lines causes loss of surface IgM expression in all tested lines by blocking N-glycan maturation and causing accumulation of immature BCR proteins, consistent with retention in the endoplasmic reticulum; rescue with wild-type CD79B restored surface CD79A and IgM with mature glycosylation, while a naturally occurring CD79B G137S mutant that disrupts CD79A/CD79B heterodimerization failed to rescue, demonstrating that CD79A/CD79B heterodimerization is required for BCR surface expression. CRISPR/Cas9 knockout of CD79A or CD79B in B lymphoma lines, rescue with WT vs. G137S mutant CD79B, N-glycan maturation analysis, surface IgM flow cytometry, ER retention assessment Journal of immunology (Baltimore, Md.: 1950) High 36426942
2004 In the avian (chicken) BCR, the cytoplasmic domain of Igalpha (CD79A ortholog) efficiently supports B cell development in precursors lacking endogenous surface Ig expression when expressed as a chimeric CD8α-Igalpha construct; by contrast, an equivalent chimeric construct containing the Igbeta cytoplasmic domain actively inhibited B cell development, demonstrating functionally distinct roles for the two cytoplasmic domains in B cell development. Retroviral gene transfer of chimeric CD8α-Igalpha or CD8α-Igbeta constructs into developing chicken B cell precursors in vivo; analysis of B cell development Immunological reviews Medium 14962183
2007 MHC class II associates with Igα/Igβ (CD79A/CD79B); mutations in the connecting peptide region of the MHC II alpha chain (but not beta chain) impair MHC II-mediated calcium mobilization and abolish co-association with Igα/Igβ, while Igβ knockdown by shRNA eliminates the MHC II-mediated calcium response but not cell death signaling. MHC II alpha chain connecting peptide mutagenesis, co-immunoprecipitation with Igα/Igβ, shRNA knockdown of Igβ, Ca2+ mobilization and cell death assays Immunology letters Medium 18194817
2021 CD79A signaling domain incorporated as a composite CD79A/CD40 co-stimulatory endodomain in CD19 CAR-T cells enhances NF-κB and p38 activation upon CD19 antigen exposure, produces superior T cell proliferation, sustained tumor suppression, and enhanced in vivo anti-tumor activity and CAR-T cell expansion compared to CD28 or 4-1BB co-stimulatory domains in a Raji mouse model. Chimeric antigen receptor T cell engineering with CD79A/CD40 endodomain, NF-κB/p38 signaling analysis, in vitro co-culture cytotoxicity and proliferation assays, in vivo Raji xenograft mouse model Molecular therapy: the journal of the American Society of Gene Therapy Medium 33940156

Source papers

Stage 0 corpus · 100 papers · ranked by NIH iCite citations
Year Title Journal Citations PMID
2011 The pathophysiology of IgA nephropathy. Journal of the American Society of Nephrology : JASN 694 21949093
2001 IgA Fc receptors. Annual review of immunology 391 12524384
2010 Selective IgA deficiency. Journal of clinical immunology 366 20101521
1988 B lymphocyte lineage-restricted expression of mb-1, a gene with CD3-like structural properties. The EMBO journal 295 2463161
2001 Predicting progression in IgA nephropathy. American journal of kidney diseases : the official journal of the National Kidney Foundation 292 11576875
2018 IgA Responses to Microbiota. Immunity 269 30134201
1974 IgA nephropathy. The American journal of pathology 256 4601708
2001 IgA and the IgA Fc receptor. Trends in immunology 221 11274926
1985 Jacalin: an IgA-binding lectin. Journal of immunology (Baltimore, Md. : 1950) 215 3871459
1993 Signal transduction by immunoglobulin is mediated through Ig alpha and Ig beta. The Journal of experimental medicine 205 7688784
2019 IgA: Structure, Function, and Developability. Antibodies (Basel, Switzerland) 200 31817406
2012 Pathogenesis of IgA nephropathy. Nature reviews. Nephrology 185 22430056
2014 The genetics and immunobiology of IgA nephropathy. The Journal of clinical investigation 175 24892706
2023 IgA nephropathy. Nature reviews. Disease primers 167 38036542
1995 CD79a: a novel marker for B-cell neoplasms in routinely processed tissue samples. Blood 151 7632952
1999 Mutations in Igalpha (CD79a) result in a complete block in B-cell development. The Journal of clinical investigation 147 10525050
2012 Corticosteroid therapy in IgA nephropathy. Journal of the American Society of Nephrology : JASN 142 22539830
1988 The immunohistology of IgA nephropathy. American journal of kidney diseases : the official journal of the National Kidney Foundation 135 3142256
2021 IgA vasculitis. Seminars in immunopathology 120 34170395
2021 Current treatment of IgA nephropathy. Seminars in immunopathology 116 34495361
2006 Treatment of IgA nephropathy. Kidney international 112 16641928
2002 Interactions of human mesangial cells with IgA and IgA-containing immune complexes. Kidney international 109 12110007
2003 Somatic hypermutation of the B cell receptor genes B29 (Igbeta, CD79b) and mb1 (Igalpha, CD79a). Proceedings of the National Academy of Sciences of the United States of America 106 12651942
2001 Peripheral T-cell lymphoma with aberrant expression of CD79a and CD20: a diagnostic pitfall. Modern pathology : an official journal of the United States and Canadian Academy of Pathology, Inc 106 11235901
2014 IgA, IgA receptors, and their anti-inflammatory properties. Current topics in microbiology and immunology 105 25116102
2018 Postmenopausal breast cancer and oestrogen associations with the IgA-coated and IgA-noncoated faecal microbiota. British journal of cancer 104 29360814
1987 IgA- and secretory IgA-opsonized S. aureus induce a respiratory burst and phagocytosis by polymorphonuclear leucocytes. Immunology 103 3610212
2004 Pathogenesis of IgA nephropathy. Seminars in nephrology 100 15156526
2021 Complement activation in IgA nephropathy. Seminars in immunopathology 92 34379175
2014 Re-thinking the functions of IgA(+) plasma cells. Gut microbes 88 25483334
1988 Proteinuria in IgA nephropathy. Kidney international 88 3367561
2004 IgA nephropathy: an update. Current opinion in nephrology and hypertension 81 15202611
1991 IgA deficiency. Immunodeficiency reviews 80 1931006
1998 Co-expression of CD79a (JCB117) and CD3 by lymphoblastic lymphoma. The Journal of pathology 79 9924428
2024 Atrasentan in Patients with IgA Nephropathy. The New England journal of medicine 74 39460694
2023 B-Cell Receptor Signaling and Beyond: The Role of Igα (CD79a)/Igβ (CD79b) in Normal and Malignant B Cells. International journal of molecular sciences 66 38203179
2009 Role of IgA and IgA fc receptors in inflammation. Journal of clinical immunology 66 19834792
1992 The B29 and mb-1 polypeptides are differentially expressed during human B cell differentiation. European journal of immunology 66 1396979
1992 Receptors for IgA on phagocytic cells. Immunologic research 64 1287121
2000 Immunoreactivity of B-cell markers (CD79a, L26) in rare cases of extranodal cytotoxic peripheral T- (NK/T-) cell lymphomas. Modern pathology : an official journal of the United States and Canadian Academy of Pathology, Inc 63 10912936
2014 MicroRNAs in IgA nephropathy. Nature reviews. Nephrology 61 24709842
2011 IgA pemphigus. Clinics in dermatology 60 21679872
2002 Isolation and detection of human IgA using a streptococcal IgA-binding peptide. Journal of immunology (Baltimore, Md. : 1950) 60 12133959
2002 Pathogenic significance of IgA receptor interactions in IgA nephropathy. Trends in molecular medicine 59 12383768
2015 Role of complement in IgA nephropathy. Journal of nephrology 58 26567162
2013 Expression of the B-cell receptor component CD79a on immature myeloid cells contributes to their tumor promoting effects. PloS one 58 24146823
1994 The expression of the B-cell marker mb-1 (CD79a) in Hodgkin's disease. Histopathology 56 7520411
2021 IgA potentiates NETosis in response to viral infection. Proceedings of the National Academy of Sciences of the United States of America 53 34183391
1988 Activation of complement in IgA nephropathy. American journal of kidney diseases : the official journal of the National Kidney Foundation 52 3055972
2023 Current understanding of IgA antibodies in the pathogenesis of IgA nephropathy. Frontiers in immunology 51 37114051
2023 Targeting complement in IgA nephropathy. Clinical kidney journal 51 38053977
2008 The role of secretory IgA and complement in IgA nephropathy. Seminars in nephrology 51 18222347
2006 The B cell receptor promotes B cell activation and proliferation through a non-ITAM tyrosine in the Igalpha cytoplasmic domain. Immunity 49 16860757
1995 Discordant expression of immunoglobulin and its associated molecule mb-1/CD79a is frequently found in mediastinal large B cell lymphomas. The American journal of pathology 48 7887454
2017 Inflammation in IgA nephropathy. Pediatric nephrology (Berlin, Germany) 47 28293726
2008 The glomerular response to IgA deposition in IgA nephropathy. Seminars in nephrology 46 18222350
2022 Mechanism of CD79A and CD79B Support for IgM+ B Cell Fitness through B Cell Receptor Surface Expression. Journal of immunology (Baltimore, Md. : 1950) 45 36426942
2019 IgA pemphigus: A systematic review. Journal of the American Academy of Dermatology 45 31812619
1990 Polymeric IgA and immune complex concentrations in IgA-related renal disease. Kidney international 43 2205751
2009 Diagnostic utility of the B-cell lineage markers CD20, CD79a, PAX5, and CD19 in paraffin-embedded tissues from lymphoid neoplasms. Applied immunohistochemistry & molecular morphology : AIMM 41 18838917
2002 CD44 expression in IgA nephropathy. American journal of kidney diseases : the official journal of the National Kidney Foundation 41 11840384
2000 Flow cytometric detection of CD79a expression in T-cell acute lymphoblastic leukemias. American journal of clinical pathology 41 10874883
1999 Elevation of serum IgA in spondyloarthropathies and IgA nephropathy and its pathogenic role. Current opinion in rheumatology 40 10411380
2010 IgA autoantibodies in the pemphigoids and linear IgA bullous dermatosis. Experimental dermatology 39 20500772
2005 Secretory IgA antibodies from plants. Current pharmaceutical design 39 16026297
1997 Size-dependent effect of IgA on the IgA Fc receptor (CD89). European journal of immunology 39 9341762
2002 Novel Igalpha (CD79a) gene mutation in a Turkish patient with B cell-deficient agammaglobulinemia. American journal of medical genetics 37 11920841
1995 Alternative splicing of CD79a (Ig-alpha/mb-1) and CD79b (Ig-beta/B29) RNA transcripts in human B cells. Molecular immunology 37 7643857
2024 Contemporary review of IgA nephropathy. Frontiers in immunology 36 39188719
2021 Composite CD79A/CD40 co-stimulatory endodomain enhances CD19CAR-T cell proliferation and survival. Molecular therapy : the journal of the American Society of Gene Therapy 35 33940156
1999 Pathogenesis of IgA nephropathy. Annales de medecine interne 34 10392257
2015 Role of IgA receptors in the pathogenesis of IgA nephropathy. Journal of nephrology 33 26572664
2012 IgA production and tonsillar focal infection in IgA nephropathy. Journal of clinical and experimental hematopathology : JCEH 33 23269075
2002 Receptor-facilitated antigen presentation requires the recruitment of B cell linker protein to Igalpha. Journal of immunology (Baltimore, Md. : 1950) 33 11859098
1993 Expression of the Ig-associated heterodimer (mb-1 and B29) in Hodgkin's disease. Histopathology 33 8454258
1977 IgA nephropathy. Human pathology 33 856715
2002 Immunohistochemical detection of CD79a expression in precursor T cell lymphoblastic lymphoma/leukaemias. The Journal of pathology 32 12115880
2020 Immunological Pattern in IgA Nephropathy. International journal of molecular sciences 31 32085673
2005 Aberrant expression of CD7, CD56, and CD79a antigens in acute myeloid leukemias. Experimental and molecular pathology 31 16005710
2022 Intrahepatic inflammatory IgA+PD-L1high monocytes in hepatocellular carcinoma development and immunotherapy. Journal for immunotherapy of cancer 30 35577505
2018 Serum IgA/C3 and glomerular C3 staining predict severity of IgA nephropathy. Pediatrics international : official journal of the Japan Pediatric Society 30 29178575
2013 IL-4 upregulates Igα and Igβ protein, resulting in augmented IgM maturation and B cell receptor-triggered B cell activation. Journal of immunology (Baltimore, Md. : 1950) 30 23776171
2005 Mechanisms of tubulointerstitial injury in IgA nephropathy. Kidney international. Supplement 30 15752226
2002 Salivary IgA subclasses and bacteria-reactive IgA in patients with aggressive periodontitis. Journal of periodontal research 30 12366855
2010 Oxidative stress in IgA nephropathy. Nephron. Clinical practice 28 20606479
2003 Pathogenesis of IgA nephropathy. Seminars in nephrology 27 14631563
2004 Basal Igalpha/Igbeta signals trigger the coordinated initiation of pre-B cell antigen receptor-dependent processes. Journal of immunology (Baltimore, Md. : 1950) 24 15240688
2023 Compromised antigen binding and signaling interfere with bispecific CD19 and CD79a chimeric antigen receptor function. Blood advances 23 36469024
1997 IgA nephropathy-specific expression of the IgA Fc receptors (CD89) on blood phagocytic cells. Clinical and experimental immunology 23 9367406
1995 The novel variants of mb-1 and B29 transcripts generated by alternative mRNA splicing. Immunology letters 23 8747711
2021 The microbiome and IgA nephropathy. Seminars in immunopathology 22 34664087
2010 The role of Ig-α/β in B cell antigen receptor internalization. Immunology letters 22 20837062
2007 MHC class II structural requirements for the association with Igalpha/beta, and signaling of calcium mobilization and cell death. Immunology letters 22 18194817
1999 Familial IgA nephropathy. Journal of nephrology 22 10493564
2020 Complement in IgA Nephropathy: The Role of Complement in the Pathogenesis, Diagnosis, and Future Management of IgA Nephropathy. Advances in chronic kidney disease 21 32553243
2006 Analysis of the individual contributions of Igalpha (CD79a)- and Igbeta (CD79b)-mediated tonic signaling for bone marrow B cell development and peripheral B cell maturation. Journal of immunology (Baltimore, Md. : 1950) 21 17114463
2004 The avian B-cell receptor complex: distinct roles of Igalpha and Igbeta in B-cell development. Immunological reviews 21 14962183
1996 Differential expression of B29 (CD79b) and mb-1 (CD79a) proteins in acute lymphoblastic leukaemia. Leukemia 21 8656670
2022 IgA vasculitis nephritis. Current opinion in pediatrics 19 35125382
2022 Chimeric Fusion between Clostridium Ramosum IgA Protease and IgG Fc Provides Long-Lasting Clearance of IgA Deposits in Mouse Models of IgA Nephropathy. Journal of the American Society of Nephrology : JASN 19 35172987

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