| First Author | Noorchashm H | Year | 1999 |
| Journal | Cell Immunol | Volume | 195 |
| Issue | 1 | Pages | 75-9 |
| PubMed ID | 10433799 | Mgi Jnum | J:56783 |
| Mgi Id | MGI:1342413 | Doi | 10.1006/cimm.1999.1522 |
| Citation | Noorchashm H, et al. (1999) Contribution of the innate immune system to autoimmune diabetes: a role for the CR1/CR2 complement receptors. Cell Immunol 195(1):75-9 |
| abstractText | 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. |
