TLR-activated B cells suppress T cell-mediated autoimmunity. - Archive ouverte HAL Access content directly
Journal Articles Journal of Immunology Year : 2008

TLR-activated B cells suppress T cell-mediated autoimmunity.

Abstract

TLR sense microbial infections, and control activation of immune responses. Dendritic cells, macrophages, and B lymphocytes express TLR and the TLR-signaling adaptor protein MyD88. The impact of TLR-activated B cells on T cell-mediated inflammation is unknown. In this study, we have used mice carrying B cell-restricted deficiencies in MyD88 or in distinct TLR to examine the impact of TLR-activated B cells on a T cell-mediated autoimmune disease, experimental autoimmune encephalomyelitis (EAE). We demonstrate that TLR-signaling in B cells suppresses inflammatory T cell responses (both Th1 and Th17), and stimulates recovery from EAE. Only certain TLR are required on B cells for resolution of EAE, and these are dispensable for disease initiation, indicating that a category of TLR agonists preferentially triggers a suppressive function in B cells and thereby limits autoimmune disease. The TLR agonists controlling the regulatory function of B cells are provided by components of Mycobacterium tuberculosis present in the adjuvant. Thus, MyD88 signaling in B cells antagonizes MyD88 signaling in other cells, which drives differentiation of Th17 cells and is required for induction of EAE. Altogether, our data indicate that B cells link recognition of microbial products via TLR to suppression of a T cell-mediated autoimmune disease.

Dates and versions

pasteur-00324528 , version 1 (25-09-2008)

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Vicky Lampropoulou, Kai Hoehlig, Toralf Roch, Patricia Neves, Elisabeth Calderón Gómez, et al.. TLR-activated B cells suppress T cell-mediated autoimmunity.. Journal of Immunology, 2008, 180 (7), pp.4763-73. ⟨10.4049/jimmunol.180.7.4763⟩. ⟨pasteur-00324528⟩
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