Summary: | <p>Abstract</p> <p>Protective responses in mice immunized with an interferon-gamma producing strain of <it>Cryptococcus neoformans</it>, H99γ, are associated with IL-17A production by neutrophils. Neutrophil depletion in H99γ-immunized mice did not affect pulmonary fungal burden, indicating that neutrophils are not required for clearance. However, we observed an increase in IL-17A in the lungs of neutrophil-depleted H99γ infected mice, which corresponded to an increase in IL-17A<sup>+</sup> γδ<sup>+</sup> T cells. Moreover, we observed increased IL-17A<sup>+</sup>/ CD3<sup>+</sup> cells and IL-17A<sup>+</sup>/γδ<sup>+</sup> cells, but decreased IL-17A<sup>+</sup>/Ly6G<sup>+</sup> neutrophils in the lungs of IL-17 receptor (R)A deficient mice compared to wild-type mice. Increased production of IL-17A in neutropenic mice coincided with increased IL-6 and CXCL1, but not Th17 inducing cytokines TGF-β, IL-21 and IL-23. Concurrent depletion of neutrophils and γδ<sup>+</sup> T cells reduced IL-17A levels. Our results suggest that γδ<sup>+</sup> T cells mediate significant IL-17A production in neutropenic mice during the protective response to <it>C</it>. <it>neoformans</it> infection.</p>
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