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CD46 delivers co-stimulatory signals for optimal CD8(+) T cell activity by augmenting nutrient-influx and fatty acid synthesis.
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Only type-I interferon restricts viral replication of attenuated Measles virus (MV) Schwarz strain in mice, independently of the presence of hCD46 receptor.
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CD46 levels were positive in 3.3% (n = 3) and negative in 96.7% (n = 90). Conclusion This study does not support the theory of measles virus as the cause of otosclerosis.
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Findings demonstrate that CD46 is a key inhibitor of complement activation whose downregulation may be involved in the pathogenesis of bullous pemphigoid.
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these data suggest a possible mechanism underlying the regulatory function of CD46 on T cells.
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study demonstratede that MMP-9-mediated shedding of CD46 is an integral part of autocrine Th1 regulation and that this pathway is dysregulated in T cells from patients with systemic lupus erythematosus
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the cell surface expression level of CD46 was markedly higher in patient myeloma cells with 1q gain than in those with normal 1q copy number.
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Our findings reveal a novel role of CD46 in accelerating inflammatory responses upon meningococcal infection or LPS stimulation by regulating the functional polarization and survival of macrophages.
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study reveals common CD46 and IFI44L SNPs associated with measles-specific humoral immunity, and highlights the importance of alternative splicing/virus cellular receptor isoform usage as a mechanism explaining inter-individual variation in immune response after live measles vaccine
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study showed no genotype differences in CD46 IVS1-1724 C>G Single nucleotide polymorphis (SNP) between Recurrent Spontaneous Abortion and fertile women
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Isoforms of CD46 impact on HHV-6B infection and thereby in part explain the distinct tropism of HHV-6AGS and HHV-6BPL1.
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This study suggests that the promoter polymorphism (rs2796267, -496 A/G) CD46 gene may be related to susceptibility of acute renal allograft rejection in Korean kidney transplantation recipients.
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provides insight into CD46 alternative splicing regulation with implications for its function in the immune system and for genetic disease
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CD46 controls both Th1 activation and regulation via a miR-150-dependent mechanism.
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Data show that CD28 antigen costimulation modulates CD46 antigen surface expression on activated T cells.
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This review summarizes our current knowledge of disease-associated mutations in this complement inhibitor(CD46).
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It was not discover any association between A304V or other CD46 SNPs and preeclampsia.
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gene deficiency results in defective Th1 cell induction due to failure in metabolic reprogramming
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Each mutant C3b bound MCP at reduced affinity, providing a molecular basis for its reduced cofactor activity in atypical hemolytic uremic syndrome.
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The mutations in the regulators CFH, CFI and MCP involve loss-of-function, whereas those for C3 involve gain-of-function.
