Institute National Of Sante Et Of La Recherche Medicale U550

Paris, France

Institute National Of Sante Et Of La Recherche Medicale U550

Paris, France
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He B.,Mount Sinai School of Medicine | Santamaria R.,Institute Municipal dInvestigacio Medica Hospital Del Mar | Xu W.,Mount Sinai School of Medicine | Cols M.,Mount Sinai School of Medicine | And 28 more authors.
Nature Immunology | Year: 2010

BAFF and APRIL are innate immune mediators that trigger immunoglobulin G (IgG) and IgA class-switch recombination (CSR) in B cells by engaging the receptor TACI. The mechanism that underlies CSR signaling by TACI remains unknown. Here we found that the cytoplasmic domain of TACI encompasses a conserved motif that bound MyD88, an adaptor that activates transcription factor NF-κB signaling pathways via a Toll-interleukin 1 (IL-1) receptor (TIR) domain. TACI lacks a TIR domain, yet triggered CSR via the DNA-editing enzyme AID by activating NF-κB through a Toll-like receptor (TLR)-like MyD88-IRAK1-IRAK4-TRAF6-TAK1 pathway. TACI-induced CSR was impaired in mice and humans lacking MyD88 or the kinase IRAK4, which indicates that MyD88 controls a B cell-intrinsic, TIR-independent, TACI-dependent pathway for immunoglobulin diversification. © 2010 Nature America, Inc. All rights reserved.

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