We appreciate the thoughtful commentary from Zhu et al. (1) regarding our study on B lymphocytes and regulatory T cells (Tregs) in type 1 diabetes and islet transplantation (2). We are pleased that they highlight our central observations in the NOD background, including the ability of B-cell deficiency to permit anti-CD45RB–mediated tolerance in the autoimmune type 1 diabetes background, the expansion of Helios-positive Tregs, improved Treg-to-effector ratios within insulin-reactive compartments that suggests a role for B lymphocytes in shaping Treg specificity, and enhanced suppressive function associated with GARP expression. We agree that these results support a model in which B cells antagonize immune regulation.
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