Affinage

CD93

Complement component C1q receptor · UniProt Q9NPY3

Length
652 aa
Mass
68.6 kDa
Annotated
2026-04-28
62 papers in source corpus 18 papers cited in narrative 18 extracted findings

Mechanistic narrative

Synthesis pass · prose summary of the discoveries below

CD93 is a type I transmembrane glycoprotein expressed on myeloid cells, endothelial cells, and platelets that functions as a receptor for defense collagens (C1q, MBL, SP-A) to modulate phagocytosis, apoptotic cell clearance, and vascular immune trafficking. Its extracellular region contains a C-type lectin domain and EGF-like repeats, while its cytoplasmic tail recruits the ERM protein moesin and the PDZ adaptor GIPC to transduce phagocytic and PTK/MAPK-dependent signaling (PMID:9047234, PMID:15819698, PMID:15459234, PMID:11531942). O-glycosylation is required for stable surface expression, and metalloproteinase-dependent ectodomain shedding releases soluble CD93 into plasma (PMID:12891708, PMID:16002728). On tumor vasculature, CD93 suppresses ICAM1/VCAM1 expression and CCL21 secretion, limiting effector T-cell infiltration; its blockade promotes vascular normalization and enhances anti-tumor immunity (PMID:39805660, PMID:38250037).

Mechanistic history

Synthesis pass · year-by-year structured walk · 10 steps
  1. 1994 High

    Identifying CD93 as a distinct phagocyte surface receptor that modulates C1q-mediated phagocytic enhancement resolved a long-sought question about which molecule linked complement recognition to ingestion.

    Evidence mAb-based immunoprecipitation and phagocytosis inhibition on monocytes and neutrophils; C1q-Sepharose affinity precipitation from surface-iodinated PMN

    PMID:7911495 PMID:8144968

    Open questions at the time
    • Molecular identity of the receptor not yet determined at cDNA level
    • Relationship between co-immunoprecipitated CD43 and CD93 function unresolved
    • No intracellular signaling pathway identified
  2. 1997 High

    Cloning CD93 revealed a novel domain architecture—C-type lectin CRD, five EGF-like repeats, transmembrane segment, and short cytoplasmic tail—establishing it as a new class of innate immune receptor rather than a classical complement receptor.

    Evidence cDNA cloning from human monocyte library, protein purification via inhibitory mAbs R3/R139, amino acid sequencing

    PMID:9047234

    Open questions at the time
    • Ligand-binding domain within CD93 not mapped
    • No structural information on CRD or EGF domains
    • Intracellular signaling mechanism unknown
  3. 1999 High

    Demonstrating that cross-linking CD93 alone (without C1q) enhances phagocytosis and that O-glycosylation accounts for anomalous gel migration established CD93 as a direct signaling receptor rather than a passive C1q-docking site.

    Evidence Glycosylation inhibitors, glycosidases, in vitro translation, mAb cross-linking phagocytosis assay on monocytes

    PMID:10092817

    Open questions at the time
    • Downstream signaling pathway not identified
    • Identity of intracellular effectors unknown
  4. 2001 Medium

    Multiple studies defined the functional scope of CD93: it mediates C1q/MBL/SP-A-enhanced phagocytosis in microglia (including amyloid-β clearance), signals through PTK/MAPK on endothelial cells to induce IL-8, and is predominantly expressed on endothelium in tissues—shifting the perceived role from purely myeloid to also endothelial.

    Evidence Microglial phagocytosis assays with intracellular anti-CD93 antibody electroporation; mAb cross-linking plus kinase inhibitor experiments on HUVEC; immunohistochemistry with domain-specific antibodies; recombinant MBL mutagenesis identifying GEKGEP binding motif

    PMID:10648005 PMID:11390503 PMID:11531942 PMID:11533031 PMID:11698500

    Open questions at the time
    • Direct binding of C1q collagen-like region to CD93 ectodomain not demonstrated with purified proteins
    • Structural basis for GEKGEP recognition unknown
    • PTK/MAPK pathway components downstream of CD93 not fully mapped
  5. 2003 High

    Showing that O-glycosylation is required for stable CD93 surface expression explained how post-translational processing gates receptor availability and potentially regulates phagocytic competence.

    Evidence Glycosylation inhibitor BAG treatment in U937 cells and reversible ldlD CHO cell system with metabolic labeling

    PMID:12891708

    Open questions at the time
    • Specific O-glycan sites not mapped
    • Whether glycosylation affects ligand binding affinity unknown
  6. 2004 High

    CD93 knockout mice revealed that CD93 is required for in vivo apoptotic cell clearance but dispensable for C1q-dependent complement/FcγR phagocytosis, decoupling CD93 from classical complement pathways and repositioning it as an efferocytosis regulator.

    Evidence CD93-null mice, in vivo peritoneal apoptotic cell clearance assay, in vitro phagocytosis controls

    PMID:15004139

    Open questions at the time
    • Mechanism by which CD93 promotes apoptotic cell clearance in vivo not determined
    • Whether CD93 directly recognizes eat-me signals on apoptotic cells unknown
  7. 2005 High

    Identification of moesin and GIPC as cytoplasmic tail binding partners, with positively charged juxtamembrane residues mediating moesin binding and a C-terminal PDZ motif recruiting GIPC, provided the first molecular model for how CD93 connects to the actin cytoskeleton and phagocytic signaling.

    Evidence Yeast two-hybrid, GST pulldown, co-capping in monocytes, PIP2 modulation, cell-permeable peptide phagocytosis assay

    PMID:15459234 PMID:15819698

    Open questions at the time
    • Whether moesin and GIPC bind simultaneously or competitively not resolved
    • Downstream effectors of GIPC in the phagocytic pathway not identified
  8. 2005 High

    Demonstrating metalloproteinase-dependent ectodomain shedding upon inflammatory stimuli and detection of soluble CD93 in plasma established regulated proteolysis as a mechanism for modulating CD93 activity and generating a circulating form.

    Evidence Western blot, ELISA, metalloproteinase inhibitor (1,10-phenanthroline), detection of sCD93 in human plasma

    PMID:16002728

    Open questions at the time
    • Identity of the responsible metalloproteinase unknown (ADAM17 excluded)
    • Biological function of soluble CD93 not established
    • Fate and signaling role of the intracellular cleavage fragment unclear
  9. 2024 Medium

    Discovery that CD93 on pleural mesothelial cells suppresses CCL21 secretion to limit dendritic cell migration and systemic anti-tumor immunity revealed an unexpected immunosuppressive role outside the vascular endothelium.

    Evidence RNA-Seq, miRNA array, siRNA knockdown, chemotaxis assay, luciferase reporter, in vivo tumor models

    PMID:38250037

    Open questions at the time
    • Mechanism by which CD93 represses CCL21 transcription or secretion not defined
    • Relevance to non-tumor pleural biology unknown
    • Single-lab finding
  10. 2025 Medium

    Showing that anti-CD93 blockade upregulates ICAM1/VCAM1 on tumor vasculature and synergizes with adoptive T-cell therapy established CD93 as a targetable vascular immune checkpoint controlling effector T-cell infiltration.

    Evidence In vivo mouse melanoma models, anti-CD93 mAb, ICAM1/VCAM1 neutralizing antibodies, CAR-T combination therapy

    PMID:39805660

    Open questions at the time
    • How CD93 signaling suppresses adhesion molecule expression mechanistically is unknown
    • Human tumor vascular expression and clinical relevance not yet validated
    • Whether this function depends on the same cytoplasmic signaling as phagocytic enhancement is unexplored

Open questions

Synthesis pass · forward-looking unresolved questions
  • The metalloproteinase responsible for CD93 shedding, the biological function of soluble CD93 and the intracellular cleavage fragment, the structural basis of defense collagen recognition, and the signaling cascade by which endothelial CD93 suppresses adhesion molecule expression remain unresolved.
  • Identity of the sheddase
  • Crystal or cryo-EM structure of CD93 ectodomain
  • Mechanism linking CD93 to ICAM1/VCAM1 transcriptional regulation

Mechanism profile

Synthesis pass · controlled-vocabulary classification · explore literature graph →
Molecular activity
GO:0060089 molecular transducer activity 3 GO:0060090 molecular adaptor activity 2
Localization
GO:0005886 plasma membrane 6 GO:0005576 extracellular region 1
Pathway
R-HSA-168256 Immune System 5 R-HSA-162582 Signal Transduction 3
Partners
C1QAGIPC1MBL2MSNSFTPA1

Evidence

Reading pass · 18 per-paper findings extracted from the source corpus
Year Finding Method Journal Conf PMIDs
1997 CD93 (C1qR(P)) was cloned and identified as a novel type I transmembrane protein with a C-type carbohydrate recognition domain, five EGF-like domains, a transmembrane domain, and a short cytoplasmic tail. Monoclonal antibodies R3 and R139 that inhibit C1q/MBL/SPA-mediated enhancement of phagocytosis were used to purify and identify this 126 kDa cell surface protein as the receptor mediating phagocytic enhancement. cDNA cloning, protein purification by mAb affinity, amino acid sequencing, anti-peptide antiserum validation Immunity High 9047234
1999 CD93 (C1qRP) is a heavily O-glycosylated protein, and direct cross-linking of CD93 with immobilized anti-CD93 mAb R3 on human monocytes triggers enhanced phagocytic capacity in the absence of C1q ligand, demonstrating direct involvement of CD93 in regulating phagocytosis. O-linked glycosylation accounts for much of the difference between predicted molecular weight and SDS-PAGE migration. Glycosylation inhibitors, specific glycosidases, in vitro translation, CHO cell transfection, phagocytosis assay with mAb cross-linking Journal of immunology High 10092817
1998 CD93 (C1qRP) expression is restricted to cells of myeloid lineage and endothelial cells (and platelets), but is absent in lymphoid cells, HeLa epithelial cells, and fibroblasts, establishing cell-type specificity of CD93-mediated phagocytic enhancement. Northern blot, RT-PCR, FACS analysis with mAbs R139 and R3 Journal of immunology High 9469455
2004 CD93-deficient mice show a significant defect in the in vivo clearance of apoptotic cells (both human Jurkat T cells and murine thymocytes) from the inflamed peritoneum, but CD93 is not required for C1q-mediated enhancement of complement- or FcγR-dependent phagocytosis in vitro or in vivo. CD93 knockout mice, in vivo apoptotic cell clearance assay, in vitro phagocytosis assays, intravital microscopy Journal of immunology High 15004139
2004 CD93 interacts with the PDZ domain-containing adaptor protein GIPC through a class I PDZ-binding domain in the CD93 carboxyl terminus, with four positively charged amino acids in the juxtamembrane domain critical for stabilizing this interaction. A cell-permeable peptide encoding the C-terminal 11 amino acids of CD93 enhances phagocytosis, implicating this interaction in the modulation of phagocytic activity. Yeast two-hybrid screen, in vitro GST fusion protein-binding assay, cell-permeable peptide treatment, phagocytosis assay Journal of leukocyte biology High 15459234
2005 CD93 ectodomain shedding from human monocytes and neutrophils is induced by phorbol dibutyrate, TNF-α, and LPS in a metalloproteinase-dependent but ADAM17-independent manner. The shed soluble form retains the N-terminal CRD and EGF repeats. Cross-linking CD93 on monocytes also triggers shedding with generation of intracellular domain-containing cleavage products. Soluble CD93 is detectable in human plasma, confirming physiological relevance. Western blot, ELISA, metalloproteinase inhibitor (1,10-phenanthroline), flow cytometry, detection of sCD93 in human plasma Journal of immunology High 16002728
2005 The intracellular protein moesin binds to the cytoplasmic tail of CD93, with the binding site mapping to the first four positively charged amino acids in the juxtamembrane region of the CD93 cytoplasmic tail. Co-capping of moesin with CD93 in human monocytes confirmed the association within intact cells. Moesin binding to CD93 is enhanced by phosphatidylinositol 4,5-bisphosphate (PIP2) and modulated by binding of other intracellular molecules to the C-terminal 11 amino acids. GST fusion protein pulldown with cell lysates and recombinant moesin, co-capping in human monocytes, deletion mutant analysis, PIP2 addition assay Immunology High 15819698
2003 O-glycosylation is required for stable cell surface expression of CD93/C1qRP. Inhibition of O-glycosylation in U937 cells or in ldlD cells with a reversible glycosylation defect causes CD93 to be rapidly released into culture media or degraded rather than stably expressed on the cell surface. Glycosylation inhibitor (BAG) treatment, ldlD CHO cell transfection with reversible glycosylation defect, metabolic labeling, Western blot Journal of cellular physiology High 12891708
2001 C1qR(P)/CD93 expressed on microglia mediates C1q-enhanced phagocytosis of IgG-coated targets via its cytoplasmic domain. Introduction of an antibody against the C-terminal cytoplasmic domain of C1qRP into microglia by electroporation markedly diminished C1q-enhanced uptake of IgG-coated targets, demonstrating the necessity of the intracellular domain for signaling. Flow cytometry, immunocytochemistry, phagocytosis assay, electroporation of intracellular anti-CD93 antibody Journal of leukocyte biology Medium 10648005
2000 The murine homolog of C1qR(P)/CD93 shares identical cell-type expression pattern with the human gene (expressed in myeloid cells but not epithelial cells), and murine myeloid cells respond to C1q with enhancement of phagocytosis. A polyclonal antibody to a peptide in the intracellular domain inhibited C1q-enhanced phagocytosis only when cells were permeabilized, confirming the intracellular C-terminus is required for signal transduction. Northern blot, RT-PCR, Western blot, FACS, permeabilized-cell phagocytosis inhibition assay, chromosomal synteny analysis Molecular immunology Medium 11074255
2001 C1qR(P)/CD93 mediates enhancement of microglial uptake of C1q-opsonized amyloid beta-IgG immune complexes when IgG is at suboptimal levels. MBL and lung surfactant protein A, other ligands of C1qR(P), similarly enhanced ingestion, implicating C1qR(P) as a common receptor for defense collagens that promotes phagocytosis. In vitro phagocytosis assay with microglia, mAb inhibition of C1qR(P), comparison with MBL and SP-A ligands Journal of immunology Medium 11390503
2001 C1q-bearing immune complexes (but not monomeric C1q) induce IL-8 secretion in human umbilical vein endothelial cells through protein tyrosine kinase (PTK)- and MAPK-dependent signaling, mediated by the 126 kDa phagocytic C1q receptor (CD93). Cross-linking mAb R3 against CD93 also stimulated IL-8 production, and IL-8 induction was blocked by the PTK inhibitor genistein and the MAPK inhibitor UO126. Northern blot for IL-8 mRNA, ELISA for IL-8 protein, kinase inhibitors (genistein, UO126), mAb R3 cross-linking Clinical and experimental immunology Medium 11531942
2001 CD93/C1qR(P) is predominantly expressed on endothelial cells in human tissues (as well as neutrophils), while it is absent in most tissue macrophages. Down-regulation of CD93 occurs as blood monocytes differentiate to dendritic cells in vitro. Polyclonal antibodies to N- and C-terminal peptides, immunohistochemistry, in vitro monocyte-to-dendritic cell differentiation with flow cytometry Journal of leukocyte biology Medium 11698500
2001 The specific collagen-like sequence GEKGEP (consensus GE(K/Q/R)GEP) within MBL is critical for triggering phagocytic enhancement via C1qR(P)/CD93. MBL mutants with deletion of GXY triplets including this motif failed to enhance phagocytosis, identifying the ligand binding site on the defense collagen that interacts with CD93. Recombinant wild-type and mutant MBL expressed in baculovirus/Sf9 cells, phagocytosis assay with human peripheral blood monocytes Journal of biological chemistry Medium 11533031
1994 CD93/C1qR(P) is a cell surface protein on phagocytic cells (monocytes, neutrophils, U937 cells) that modulates C1q-mediated enhancement of phagocytosis. Three mAbs (R139, R3, U40.3) identify this as a 100 kDa (126 kDa reduced) protein that co-immunoprecipitates with CD43, suggesting a multi-subunit structure. R3 and R139 (but not U40.3) inhibit phagocytosis enhancement, while R3 also partially inhibits C1q binding. Immunoprecipitation, Western blot, mAb inhibition of phagocytosis, radioligand binding inhibition studies Journal of immunology High 8144968
1994 CD93/C1qR expressed on PMN (neutrophils) is a 125 kDa (135 kDa reduced) protein that can be affinity precipitated from surface-iodinated PMN using C1q-Sepharose. FMLP rapidly up-regulates CD93 surface expression up to fivefold from an intracellular pool, a process dependent on normal microtubule functioning (inhibited by taxol). C1q-Sepharose affinity precipitation, flow cytometry, phorbol ester and FMLP stimulation, taxol inhibition, surface iodination Journal of immunology Medium 7911495
2025 CD93 blockade in tumor vasculature increases expression of adhesion molecules ICAM1 and VCAM1, promotes tumor vascular maturation, and improves effector T-cell infiltration into solid tumors. Anti-CD93 selectively promotes T-cell infiltration in tumors where the CD93 pathway is upregulated, and synergizes with adoptive T-cell transfer to inhibit tumor progression. Neutralizing antibodies against ICAM1 and VCAM1 were used to confirm their involvement. In vivo mouse melanoma model with anti-CD93 mAb treatment, immunofluorescent staining for vascular maturation markers, flow cytometry for tumor-infiltrating lymphocytes, neutralizing antibodies against ICAM1 and VCAM1, CAR-T cell therapy combination Journal for immunotherapy of cancer Medium 39805660
2024 CD93 in pleural mesothelial cells suppresses CCL21 secretion, thereby reducing dendritic cell migration to the tumor and suppressing systemic anti-tumor T-cell responses. Tumor extracellular vesicle-derived miR-5110 downregulates pMC CD93 to promote CCL21 secretion, while C1q suppresses CD93-mediated CCL21 secretion. CD93-blocking antibodies inhibit tumor angiogenesis and promote CCL21 secretion, overcoming resistance to anti-PD-1 therapy. RNA-Seq, miRNA array, luciferase reporter assay, siRNA knockdown, endothelial tube formation assay, chemotaxis assay, recombinant proteins, flow cytometry, EV labeling and uptake assays Theranostics Medium 38250037

Source papers

Stage 0 corpus · 62 papers · ranked by NIH iCite citations
Year Title Journal Citations PMID
2000 C1q: structure, function, and receptors. Immunopharmacology 395 10904115
1997 cDNA cloning and primary structure analysis of C1qR(P), the human C1q/MBL/SPA receptor that mediates enhanced phagocytosis in vitro. Immunity 206 9047234
2002 C1qRp defines a new human stem cell population with hematopoietic and hepatic potential. Proceedings of the National Academy of Sciences of the United States of America 136 12140365
1993 Platelet activation by C1q results in the induction of alpha IIb/beta 3 integrins (GPIIb-IIIa) and the expression of P-selectin and procoagulant activity. The Journal of experimental medicine 126 7688027
2004 Murine CD93 (C1qRp) contributes to the removal of apoptotic cells in vivo but is not required for C1q-mediated enhancement of phagocytosis. Journal of immunology (Baltimore, Md. : 1950) 116 15004139
1994 Human T cells express specific binding sites for C1q. Role in T cell activation and proliferation. Journal of immunology (Baltimore, Md. : 1950) 100 8046223
1998 C1qRP, the C1q receptor that enhances phagocytosis, is detected specifically in human cells of myeloid lineage, endothelial cells, and platelets. Journal of immunology (Baltimore, Md. : 1950) 99 9469455
1994 Calreticulin is released from activated neutrophils and binds to C1q and mannan-binding protein. Clinical immunology and immunopathology 96 8062452
1994 Cell-surface protein identified on phagocytic cells modulates the C1q-mediated enhancement of phagocytosis. Journal of immunology (Baltimore, Md. : 1950) 96 8144968
2001 Antibody-mediated phagocytosis of the amyloid beta-peptide in microglia is differentially modulated by C1q. Journal of immunology (Baltimore, Md. : 1950) 89 11390503
1984 Identification of the Raji cell membrane-derived C1q inhibitor as a receptor for human C1q. Purification and immunochemical characterization. The Journal of experimental medicine 80 6436431
2021 NOT-Gated CD93 CAR T Cells Effectively Target AML with Minimized Endothelial Cross-Reactivity. Blood cancer discovery 78 34778803
1997 The C1q and collectin binding site within C1q receptor (cell surface calreticulin). Immunopharmacology 78 9476117
2005 CD93 is rapidly shed from the surface of human myeloid cells and the soluble form is detected in human plasma. Journal of immunology (Baltimore, Md. : 1950) 73 16002728
1995 Murine mast cells express two types of C1q receptors that are involved in the induction of chemotaxis and chemokinesis. Journal of immunology (Baltimore, Md. : 1950) 67 7650391
2000 Structural and functional evidence for microglial expression of C1qR(P), the C1q receptor that enhances phagocytosis. Journal of leukocyte biology 63 10648005
1999 C1qRP is a heavily O-glycosylated cell surface protein involved in the regulation of phagocytic activity. Journal of immunology (Baltimore, Md. : 1950) 58 10092817
2001 Identification of a site on mannan-binding lectin critical for enhancement of phagocytosis. The Journal of biological chemistry 57 11533031
1993 Isolation of a human endothelial cell C1q receptor (C1qR). Journal of leukocyte biology 54 8445329
1990 Platelet C1q receptor interactions with collagen- and C1q-coated surfaces. Journal of immunology (Baltimore, Md. : 1950) 54 2212670
1997 The C1q-binding cell membrane proteins cC1q-R and gC1q-R are released from activated cells: subcellular distribution and immunochemical characterization. Clinical immunology and immunopathology 52 9191880
1990 Interaction of C1q with its receptor on cultured cell lines induces an anti-proliferative response. Clinical immunology and immunopathology 51 2293904
2001 C1qR(P), a myeloid cell receptor in blood, is predominantly expressed on endothelial cells in human tissue. Journal of leukocyte biology 47 11698500
1996 Localisation of the C1q binding site within C1q receptor/calreticulin. FEBS letters 47 8955356
2021 C1q binding to surface-bound IgG is stabilized by C1r2s2 proteases. Proceedings of the National Academy of Sciences of the United States of America 44 34155115
1991 Complement component C1q and its receptor are involved in the interaction of human sperm with zona-free hamster eggs. Molecular reproduction and development 43 1878225
1988 Reversible biotinylation of C1q with a cleavable biotinyl derivative. Application in C1q receptor (C1qR) purification. Journal of immunological methods 41 3259972
2004 CD93 interacts with the PDZ domain-containing adaptor protein GIPC: implications in the modulation of phagocytosis. Journal of leukocyte biology 39 15459234
2011 Plasma CD93 concentration is a potential novel biomarker for coronary artery disease. Journal of internal medicine 37 21332844
1990 Participation of C1q and its receptor in adherence of human diploid fibroblast. Journal of immunology (Baltimore, Md. : 1950) 37 2212651
2005 Modulated interaction of the ERM protein, moesin, with CD93. Immunology 36 15819698
1999 Up-regulation of endothelial cell binding proteins/receptors for complement component C1q by inflammatory cytokines. The Journal of laboratory and clinical medicine 36 10360628
2000 Characterization and molecular cloning of rat C1qRp, a receptor on NK cells. European journal of immunology 33 11093152
2003 Cell surface expression of C1qRP/CD93 is stabilized by O-glycosylation. Journal of cellular physiology 32 12891708
2015 CD93 gene polymorphism is associated with disseminated colorectal cancer. International journal of colorectal disease 30 26008729
2010 A gC1qR prevents white spot syndrome virus replication in the freshwater crayfish Pacifastacus leniusculus. Journal of virology 29 20686021
2016 Elevated expression of CD93 promotes angiogenesis and tumor growth in nasopharyngeal carcinoma. Biochemical and biophysical research communications 28 27255994
1988 Identification and partial characterization of human platelet C1q binding sites. Journal of immunology (Baltimore, Md. : 1950) 27 3183380
1986 Production and characterization of a murine monoclonal IgM antibody to human C1q receptor (C1qR). Journal of immunology (Baltimore, Md. : 1950) 27 3487576
1994 Regulation of C1q receptor expression on human polymorphonuclear leukocytes. Journal of immunology (Baltimore, Md. : 1950) 23 7911495
1994 Characterization of the human neutrophil C1q receptor and functional effects of free ligand on activated neutrophils. Blood 23 8068954
2016 Soluble CD93 as a Novel Biomarker in Asthma Exacerbation. Allergy, asthma & immunology research 19 27334785
2016 Whole Transcriptome Profiling Identifies CD93 and Other Plasma Cell Survival Factor Genes Associated with Measles-Specific Antibody Response after Vaccination. PloS one 19 27529750
1992 Smooth muscle and epithelial cells express specific binding sites for the C1q component of complement. Clinical immunology and immunopathology 19 1591883
2001 C1q-bearing immune complexes induce IL-8 secretion in human umbilical vein endothelial cells (HUVEC) through protein tyrosine kinase- and mitogen-activated protein kinase-dependent mechanisms: evidence that the 126 kD phagocytic C1q receptor mediates immune complex activation of HUVEC. Clinical and experimental immunology 18 11531942
2016 Soluble CD93 Is Involved in Metabolic Dysregulation but Does Not Influence Carotid Intima-Media Thickness. Diabetes 17 27659228
1999 Cloning of the mouse homolog of the 126-kDa human C1q/MBL/SP-A receptor, C1qR(p). Mammalian genome : official journal of the International Mammalian Genome Society 16 10430665
2000 Characterization of the murine homolog of C1qR(P): identical cellular expression pattern, chromosomal location and functional activity of the human and murine C1qR(P). Molecular immunology 15 11074255
1993 The C1q-R participates in immunoregulation and signal transduction. Behring Institute Mitteilungen 15 8172572
2020 Soluble CD93 in allergic asthma. Scientific reports 14 31941986
2012 Augmented production of soluble CD93 in patients with systemic sclerosis and clinical association with severity of skin sclerosis. The British journal of dermatology 14 22540233
1992 Short amino acid sequences derived from C1q receptor (C1q-R) show homology with the alpha chains of fibronectin and vitronectin receptors and collagen type IV. Journal of leukocyte biology 14 1377218
2020 Significance of Soluble CD93 in Type 2 Diabetes as a Biomarker for Diabetic Nephropathy: Integrated Results from Human and Rodent Studies. Journal of clinical medicine 13 32397261
2025 CD93 blockade promotes effector T-cell infiltration and facilitates adoptive cell therapy in solid tumors. Journal for immunotherapy of cancer 9 39805660
2024 Blockade of CD93 in pleural mesothelial cells fuels anti-lung tumor immune responses. Theranostics 8 38250037
2022 CD93 is Associated with Glioma-related Malignant Processes and Immunosuppressive Cell Infiltration as an Inspiring Biomarker of Survivance. Journal of molecular neuroscience : MN 8 36006582
2021 CD93 has a crucial role in pathogenesis of psoriasis. Journal of cosmetic dermatology 5 34028163
2022 Determining biomarkers for evaluation and diagnosis of hereditary angioedema. Clinical and translational allergy 4 36254341
2023 CD93 serves as a potential biomarker of gastric cancer and correlates with the tumor microenvironment. World journal of clinical cases 3 36818626
2024 Immuno-PET Imaging of CD93 Expression with 64Cu-Radiolabeled NOTA-mCD93 ([64Cu]Cu-NOTA-mCD93) and Insulin-Like Growth Factor Binding Protein 7 ([64Cu]Cu-NOTA-IGFBP7). Molecular pharmaceutics 1 39533706
2025 CD93: A Promising NETs-Related Biomarker for Diagnosis and Therapy in Actinic Keratosis. OncoTargets and therapy 0 40901493
2022 Amniotic fluid soluble CD93 is elevated in the presence of intra-amniotic inflammation in preterm prelabor rupture of the fetal membranes. Ceska gynekologie 0 36543585