TGF-βs play an integral role regulating both innate and adaptive immune responses. TGF-β potentiates the differentiation of CD8 T cells whereas it inhibits NK cell differentiation, induces IgA isotype switching during humoral immune responses and regulates the activation and proliferation of lymphocytes and antigen presenting cells. In addition, TGF-β1 deficiency results in the development of an early lethal autoimmune syndrome in mice mediated by CD4 T cells. To understand the mechanisms involved in the regulation of TGFβ in the immune system, here we have explored the role of BAMBI (BMP and Activin Membrane Bound Inhibitor), a transmembrane protein that inhibits both TGF-β type I and type II receptors, in the distribution of immune cells in primary and secondary lymphoid organs. By flow cytometry we demonstrate that: 1) the deficiency of BAMBI is associated with a reduction in the marginal B cell population in the spleen; 2) the deficiency of BAMBI affects the differentiation of DP and CD8 T cell populations in the thymus; 3) this altered thymic development does not affect mature peripheral T cell populations; and 4) BAMBI-KO mice exhibit an increased number of spleen NK cells. Altogether, our results point to BAMBI as a regulator of TGF-β activity in the immune system.
