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Contribution of the innate immune system to autoimmune diabetes: a role for the CR1/CR2 complement receptors.

Noorchashm H, Moore DJ, Lieu YK, Noorchashm N, Schlachterman A, Song HK, Barker CF, Naji A
Cell Immunol. 1999 195 (1): 75-9

PMID: 10433799 · DOI:10.1006/cimm.1999.1522

B lymphocytes are required for diabetogenesis in nonobese diabetic (NOD) mice. The complement component of the innate immune system regulates B cell activation and tolerance through complement receptors CR1/CR2. Thus, it is important to assess the contribution of complement receptors to autoimmune diabetes in NOD mice. Examination of the lymphoid compartments of NOD mice revealed striking expansion of a splenic B cell subset with high cell surface expression of CR1/CR2. This subset of B cells exhibited an enhanced C3 binding ability. Importantly, long-term in vivo blockade of C3 binding to CR1/CR2 prevented the emergence of the CR1/CR2(hi) B cells and afforded resistance to autoimmune diabetes in NOD mice. These findings implicate complement as an important regulatory element in controlling the T cell-mediated attack on islet beta cells of NOD mice.

Copyright 1999 Academic Press.

MeSH Terms (13)

Animals B-Lymphocytes Complement C3 Diabetes Mellitus, Type 1 Immunity, Innate Immunophenotyping Mice Mice, Inbred BALB C Mice, Inbred C57BL Mice, Inbred NOD Receptors, Complement 3b Receptors, Complement 3d Spleen

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