TLR-mediated B cell activation results in ectopic CLIP expression that promotes B cell-dependent inflammation.

Journal of Leukocyte Biology
M K NewellJ P Antel

Abstract

Infectious pathogens produce compounds called Toll ligands that activate TLRs on lymphocytes. Acute activation triggered by certain TLRs appears to "jump start" the innate immune response, characterized by the release of inflammatory cytokines and cellular expansion. In some individuals, there is a failure to control acute inflammation, resulting in postinfectious, chronic inflammation. Susceptibility to chronic inflammation is strongly associated with an individual's MHC genes. Recent clinical trials for several autoimmune diseases characterized by chronic inflammation suggest that B lymphocyte depletion therapies dampen chronic immune activation. However, currently, there is no known mechanism that accounts for the correlation among TLR activation, MHC genetics, and a pathological role for B-lymphocytes. Our hypothesis is that TLR-activated B cells (B cells that have been polyclonally activated in the absence of antigen-specific signals) are not controlled properly by T cell-dependent B cell death, thereby causing B cell-dependent chronic inflammation. Here, we show that treatment with Toll ligands results in polyclonal B cell activation accompanied by ectopic expression of CLIP. Furthermore, by adoptively transferring purifi...Continue Reading

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Citations

Aug 2, 2012·Current Infectious Disease Reports·Steven P Larosa, Steven M Opal
Sep 24, 2008·Neuroscience·B J MarshM P Stenzel-Poore
Oct 6, 2009·Biochemical Pharmacology·Jiyeon OckKyoungho Suk
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Sep 28, 2010·Experimental Gerontology·Barbara Viviani, Mariaserena Boraso
Oct 31, 2008·Journal of Neuroimmunology·Sanna RintaIrina Elovaara
Jan 22, 2015·Journal of Leukocyte Biology·Ali DivanM Karen Newell-Rogers
Jul 10, 2020·The Journal of Immunology : Official Journal of the American Association of Immunologists·Liza RijversMarvin M van Luijn

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