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CD11c + T-bet +  B cells are recognized as an important component of humoral immunity and autoimmunity. These cells can be distinguished from other B cells by their higher expression of the adenosine receptor 2a. Here we address whether A 2A  receptor activation can affect CD11c + T-bet +  B cells. We show that administration of the A 2A  receptor agonist CGS-21680 depletes established CD11c + T-bet +  B cells in ehrlichial-infected mice, in a B cell-intrinsic manner. Agonist treatment similarly depletes CD11c + T-bet +  B cells and CD138 +  B cells and reduces anti-nuclear antibodies in lupus-prone mice. Agonist treatment is also associated with reduced kidney pathology and lymphadenopathy. Moreover, A 2A  receptor stimulation depletes pathogenic lymphocytes and ameliorates disease even after disease onset, highlighting the therapeutic potential of this treatment. This study suggests that targeting the adenosine signaling pathway may provide a method for the treatment of lupus and other autoimmune diseases mediated by T-bet +  B cells.

Adenosine receptor 2a agonists target mouse CD11c+T-bet+ B cells in infection and autoimmunity