NDLI: Receptor cross-talk spatially restricts p-ERK during TLR4 stimulation of autoreactive B cells.

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Receptor cross-talk spatially restricts p-ERK during TLR4 stimulation of autoreactive B cells.

Content Provider	World Health Organization (WHO)-Global Index Medicus
Author	Kilmon, Michelle A. Roques, Jose R. Lee, Sang-Ryul Kang, Sun Ah Wagner, Nikki J. Monteith, Andrew J. Krum, Kristen N. Jones, Shannon Z. Vilen, Barbara J. Rutan, Jennifer A. Clarke, Stephen H.
Description	Country affiliation: United States Author Affiliation: Lee SR ( Department of Microbiology and Immunology, University of North Carolina, Chapel Hill, NC 27599, USA.)
Abstract	To maintain tolerance, autoreactive B cells must regulate signal transduction from the BCR and TLRs. We recently identified that dendritic cells and macrophages regulate autoreactive cells during TLR4 activation by releasing IL-6 and soluble CD40 ligand (sCD40L). These cytokines selectively repress Ab secretion from autoreactive, but not antigenically naive, B cells. How IL-6 and sCD40L repress autoantibody production is unknown. In this work, we show that IL-6 and sCD40L are required for low-affinity/avidity autoreactive B cells to maintain tolerance through a mechanism involving receptor cross-talk between the BCR, TLR4, and the IL-6R or CD40. We show that acute signaling through IL-6R or CD40 integrates with chronic BCR-mediated ERK activation to restrict p-ERK from the nucleus and represses TLR4-induced Blimp-1 and XBP-1 expression. Tolerance is disrupted in 2-12H/MRL/lpr mice where IL-6 and sCD40L fail to spatially restrict p-ERK and fail to repress TLR4-induced Ig secretion. In the case of CD40, acute signaling in B cells from 2-12H/MRL/lpr mice is intact, but the chronic activation of p-ERK emanating from the BCR is attenuated. Re-establishing chronically active ERK through retroviral expression of constitutively active MEK1 restores tolerance upon sCD40L, but not IL-6, stimulation, indicating that regulation by IL-6 requires another signaling effector. These data define the molecular basis for the regulation of low-affinity autoreactive B cells during TLR4 stimulation; they explain how autoreactive but not naive B cells are repressed by IL-6 and sCD40L; and they identify B cell defects in lupus-prone mice that lead to TLR4-induced autoantibody production.
ISSN	00221767
e-ISSN	15506606
DOI	10.4049/jimmunol.1200940
Journal	The Journal of Immunology
Issue Number	8
Volume Number	189
Language	English
Publisher	The American Association of Immunologists
Publisher Date	2012-10-15
Publisher Place	United States
Access Restriction	Open
Subject Keyword	Autoantibodies Biosynthesis B-lymphocyte Subsets Immunology Metabolism Extracellular Signal-regulated Map Kinases Lupus Nephritis Receptor Cross-talk Toll-like Receptor 4 Physiology Animals Antigens, Cd40 Pathology Cd40 Ligand Cell Nucleus Enzymology Cells, Cultured Coculture Techniques Immune Tolerance Genetics Mice Mice, Inbred C57bl Mice, Inbred Mrl Lpr Mice, Transgenic Nuclear Proteins Antagonists & Inhibitors Protein Transport Receptors, Antigen, B-cell Receptors, Interleukin-6 Signal Transduction Research Support, N.i.h., Extramural Research Support, Non-u.s. Gov't Discipline Immunology
Content Type	Text
Resource Type	Article
Subject	Immunology and Allergy Immunology

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Receptor cross-talk spatially restricts p-ERK during TLR4 stimulation of autoreactive B cells.

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Receptor cross-talk spatially restricts p-ERK during TLR4 stimulation of autoreactive B cells.