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

Hooman Noorchashm, Daniel J. Moore, Yen K. Lieu, Negin Noorchashm, Alexander Schlachterman, Howard K. Song, John D. Lambris, Clyde F. Barker, Ali Naji

    Research output: Contribution to journalArticlepeer-review

    33 Scopus citations

    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 languageEnglish (US)
    Pages (from-to)75-79
    Number of pages5
    JournalCellular Immunology
    Volume195
    Issue number1
    DOIs
    StatePublished - Jul 10 1999

    ASJC Scopus subject areas

    • Immunology

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