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题目:: Aberrant presentation of self-lipids by autoimmune B cells depletes peripheral iNKT cells.
作者:: Tan(Andy Hee-Meng),Chong(William Pooi-Kat),Ng(Sze-Wai),Basri(Nurhidayah),Xu(Shengli),Lam(Kong-Peng)
状态:: 发布时间2014-10-11 , 更新时间 2014-10-11
期刊:: Cell Rep
摘要:: Invariant natural killer T (iNKT) cells provide cognate help via CD1d to lipid antigen-presenting B cells for antibody production, but whether B cells reciprocally regulate iNKT cells remains largely unexplored. Here, we found peripheral, but not thymic, iNKT cells to be numerically reduced in autoimmune mice lacking Fas specifically in B cells. The residual iNKT cells were antigenically overstimulated, had altered cytokine production, and manifested enhanced proliferation and apoptosis. B cell-specific ablation of CD1d ameliorated these iNKT defects, suggesting that inappropriate presentation of CD1d-restricted self-lipids by autoimmune B cell-depleted peripheral iNKT cells. CD1d(+) autoimmune B cells have reduced α-galactosidase A expression and, as revealed by lipidomic profiling, altered lipidome with aberrant accumulation of certain self-lipids and reduction of others. These findings unveil a critical link between autoimmunity, B cell lipidome, and the maintenance of peripheral iNKT cells and highlight an essential homeostatic function of B cells beyond antibody production.
语言:: eng
DOI:: 10.1016/j.celrep.2014.08.043

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