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γδ T cells have been postulated to act as a first line of defense against infectious agents, particularly intracellular pathogens, representing an important link between the innate and adaptive immune responses. Human γδ T cells expand in the blood of brucellosis patients and are active against  Brucella in vitro . However, the role of γδ T cells  in vivo  during experimental brucellosis has not been studied. Here we report TCRδ −/−  mice are more susceptible to  B. abortus  infection than C57BL/6 mice at one week post-infection as measured by splenic colonization and splenomegaly. An increase in TCRγδ cells was observed in the spleens of  B. abortus -infected C57BL/6 mice, which peaked at two weeks post-infection and occurred concomitantly with diminished brucellae. γδ T cells were the major source of IL-17 following infection and also produced IFN-γ. Depletion of γδ T cells from C57BL/6, IL-17Rα −/− , and GMCSF −/−  mice enhanced susceptibility to  B. abortus  infection although this susceptibility was unaltered in the mutant mice; however, when γδ T cells were depleted from IFN-γ −/−  mice, enhanced susceptibility was observed. Neutralization of γδ T cells in the absence of TNF-α did not further impair immunity. In the absence of TNF-α or γδ T cells,  B. abortus -infected mice showed enhanced IFN-γ, suggesting that they augmented production to compensate for the loss of γδ T cells and/or TNF-α. While the protective role of γδ T cells was TNF-α-dependent, γδ T cells were not the major source of TNF-α and activation of γδ T cells following  B. abortus  infection was TNF-α-independent. Additionally, bovine TCRγδ cells were found to respond rapidly to  B. abortus  infection upon co-culture with autologous macrophages and could impair the intramacrophage replication of  B. abortus  via IFN-γ. Collectively, these results demonstrate γδ T cells are important for early protection to  B. abortus  infections.

Murine and Bovine γδ T Cells Enhance Innate Immunity against Brucella abortus Infections