Journal
JOURNAL OF IMMUNOLOGY
Volume 175, Issue 1, Pages 37-41Publisher
AMER ASSOC IMMUNOLOGISTS
DOI: 10.4049/jimmunol.175.1.37
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Funding
- NIAID NIH HHS [R01 AI053266, AI53266] Funding Source: Medline
- NIAMS NIH HHS [AR07417] Funding Source: Medline
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Polyclonal B cell activation promotes immunity without the loss of tolerance. Our data show that during activation of the innate immune system, B cell tolerance to Smith Ag Sm is maintained by dendritic cells (DCs) and macrophages (M Phi). TLR4-activated myeloid DCs and M Phi, but not plasmacytoid or lymphoid DCs, repressed autoreactive B cells through the secretion of soluble mediators, including IL-6. Although IL-6 promotes plasma cell differentiation of B cells acutely stimulated by Ag, we show that it repressed cells that were chronically exposed to self-Ag. This mechanism of tolerance was not limited to Smith Ag-specific B cells as hen egg lysozyme- and p-azophenylarsonate-specific B cells were similarly affected. Our data define a tolerogenic rolefor M Phi and DCs in regulating autoreactive B cells during activation of the innate immune system.
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