Roles of myeloid-derived suppressor cells (MDSCs) in the modulation of protective immunity against coccidioidomycosis

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Presentation Time: 03:15 PM - 04:30 PM
Poster Board Number: B690
Abstract ID: 5034

Presenting Author:
Nawal Abdul-Baki , Graduate Research Assistant I at Univ. of Texas, San Antonio

Abstract:

Coccidioidomycosis, also known as Valley Fever (VF), is an endemic respiratory disease in the southwest of the United States. Annually, the CDC estimates 400,000 cases and medical costs of over 3 billion. VF is caused by Coccidioides species that infect immunocompetent and immunocompromised individuals. The vaccine-induced protective immunity against VF requires type 1 and 17 CD4⁺ helper T cells (Th1 and Th17). However, Th1 and Th17 responses are absent in patients with severe forms of coccidioidomycosis. Myeloid-derived suppressor cells (MDSCs) have been shown to suppress the proliferation and function of CD4⁺ T cells in a variety of fungal infections, including Candida albicans and Cryptococcus neoformans. Here we show the number of MDSCs was significantly upregulated in the lungs of Coccidioides-infected C57BL/6 mice on days 7 and 11 post-challenge, compared to vaccine-protected mice. MDSCs from the lungs or spleen of non-protected mice suppressed the proliferation of CD4⁺ T cells to a greater extent compared to those isolated from naïve or vaccine-protected mice. Therefore, we reveal that MDSCs contribute to the pathogenesis of Coccidioides infection by inhibiting the proliferation and activation of CD4⁺ T cells. Further research will elucidate the mechanisms of activation and recruitment of MDSCs into the infected lungs via host-receptor interactions. These data will uncover how fungal virulence regulates MDSC function leading to detrimental immune responses.