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Cell Immunol. 1999 Jul 10;195(1):75-9.

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

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Department of Surgery, University of Pennsylvania Medical Center, Philadelphia, Pennsylvania 19104, USA.

Erratum in

  • Cell Immunol 1999 Dec 15;198(2):143.


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.

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