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Human T cells induce their own regulation through activation of B cells.

Abstract : Regulatory functions for B lymphocytes have been reported in murine models of autoimmune diseases in which B-cell deficient mice were shown to exhibit exacerbated disease. The B cells responsible for the immune regulations were identified as a subpopulation of interleukin 10-secreting cells. However, the mechanism of induction and the characteristics of regulatory B cells in humans have been hardly studied. This study reports that regulation of T cell responses can be induced by B cells following CD40-dependent cognate interaction. T cell proliferation and cytokine production were differentially regulated. Thus, CD40-induced regulatory B cells partially inhibited T cell proliferation following CD40 interaction without requirement of soluble factor. In contrast, modulation of Th1 differentiation resulted from CD80- and CD86-dependent interactions and from IL-10 production. The suppressive effects were mediated by CD19(high)IgD+CD38(high)CD24(high)CD5(high) B cells and appeared to be indirect, through the induction of regulatory T cells as indicated by the appearance of Foxp3+CD4+CD25+T cells. These data suggest that activation signals from T cells initiate regulatory properties in B cells that modulate T cell responses involving regulatory T cells. Finally, studies in autoimmune patients revealed that regulation of T cell proliferation was defective in systemic lupus erythematosus but efficient in other diseases. Restoration of efficient B-cell regulatory activity could provide innovative B-cell based treatment of autoimmune diseases.
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https://hal.univ-brest.fr/hal-00771265
Contributor : Geneviève Michel <>
Submitted on : Tuesday, January 8, 2013 - 12:17:21 PM
Last modification on : Wednesday, November 29, 2017 - 2:53:52 PM

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Sébastien Lemoine, Ahsen Morva, Pierre Youinou, Christophe Jamin. Human T cells induce their own regulation through activation of B cells.. Journal of Autoimmunity, Elsevier, 2011, 36 (3-4), pp.228-38. ⟨10.1016/j.jaut.2011.01.005⟩. ⟨hal-00771265⟩

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