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Little is known regarding the function of ?? T cells, although they accumulate at sites of inflammation in infections and autoimmune disorders. We previously observed that ?? T cells in vitro are activated by Borrelia burgdorferi in a TLR2-dependent manner. We now observe that the activated ?? T cells can in turn stimulate dendritic cells in vitro to produce cytokines and chemokines that are important for the adaptive immune response. This suggested that in vivo ?? T cells may assist in activating the adaptive immune response. We examined this possibility in vivo and observed that ?? T cells are activated and expand in number during Borrelia infection, and this was reduced in the absence of TLR2. Furthermore, in the absence of ?? T cells, there was a significantly blunted response of adaptive immunity, as reflected in reduced expansion of T and B cells and reduced serum levels of anti-Borrelia antibodies, cytokines, and chemokines. This paralleled a greater Borrelia burden in ??-deficient mice as well as more cardiac inflammation. These findings are consistent with a model of ?? T cells functioning to promote the adaptive immune response during infection.