Abstract
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 β cells of NOD mice.
Original language | English (US) |
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Pages (from-to) | 75-79 |
Number of pages | 5 |
Journal | Cellular Immunology |
Volume | 195 |
Issue number | 1 |
DOIs | |
State | Published - Jul 10 1999 |
Externally published | Yes |
ASJC Scopus subject areas
- Immunology