@entity3744 + regulatory T cells control humoral XXXX by suppressing the development of long-lived plasma cells.

@entity625 @entity19 @entity9843 @entity786 @entity19149 @entity3744 @entity792
@entity3744 (+) regulatory T cells (Tregs) are crucial for maintaining T cell tolerance, but their role in humoral @entity792 remains unclear. To address this, we combined a model of autoantibody-dependent @entity625 (K/BxN) with @entity3744 mutant scurfy @entity19 to generate Treg-deficient K/BxN @entity19 , referred to as K/BxNsf @entity19 . The disease symptoms of K/BxNsf @entity19 were exacerbated, and this coincided with increases in extrafollicular Th cells, follicular Th cells, and germinal centers. Surprisingly, the K/BxNsf @entity19 exhibited an abnormal accumulation of mature plasma cells in their spleens and a corresponding loss of bone marrow plasma cells. The plasma cells were unresponsive to the bone marrow homing chemokine @entity19149 , despite normal expression of the chemokine receptor @entity9843 . Importantly, they were long-lived and less susceptible to the cytotoxic action of @entity786 . They also expressed less FcyRIIb and were less apoptotic in response to autoantigen-autoantibody immune complexes. This suggests that Tregs control plasma cell susceptibility to cell death induced by engagement of FcyRIIb with immune complexes. Direct cytotoxic effects of Tregs also contribute to the death of plasma cells. Thus, our results reveal that Tregs suppress the emergence of long-lived splenic plasma cells by affecting plasma cell-autonomous mechanisms as well as T cell help, thereby avoiding the persistence of humoral @entity792 .
