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• W2518196601 startingPage "918" @default.
• W2518196601 abstract "Antibodies are involved in the pathogenesis of many autoimmune diseases. Although the mechanisms underlying the antibody response to infection or vaccination are reasonably well understood, we still have a poor understanding of the nature of autoimmune antibody responses. The most well studied are the anti-nuclear antibody responses characteristic of systemic lupus erythematosus and studies over the past decade or so have demonstrated a critical role for signaling by TLR7 and/or TLR9 in B cells to promote these responses. These Toll-like receptors (TLRs) can promote T-cell-independent extrafollicular antibody responses with a heavy-chain class switch and a low degree of somatic mutation, but they can also strongly boost the germinal center response that gives rise to high-affinity antibodies and long-lived plasma cells. TLRs have been shown to enhance affinity maturation in germinal center responses to produce high-affinity neutralizing antibodies in several virus infection models of mice. Although more data are needed, it appears that anti-nuclear antibodies in mouse models of lupus and in lupus patients can be generated by either pathway, provided there are genetic susceptibility alleles that compromise B-cell tolerance at one or another stage. Limited data in other autoimmune diseases suggest that the germinal center response may be the predominant pathway leading to autoantibodies in those diseases. A better understanding of the mechanisms of autoantibody production may ultimately be helpful in the development of targeted therapeutics for lupus or other autoimmune diseases." @default.
• W2518196601 created "2016-09-16" @default.
• W2518196601 creator A5080849379 @default.
• W2518196601 date "2016-10-11" @default.
• W2518196601 modified "2023-10-18" @default.
• W2518196601 title "Germinal centers and autoimmune disease in humans and mice" @default.
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• W2518196601 doi "https://doi.org/10.1038/icb.2016.78" @default.
• W2518196601 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/5663225" @default.

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