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I have been involved in the study of the host response to the pathogenic fungus, Histoplasma capsulatum for over 25 years. I have devoted the large majority of our work on the role of the innate and adaptive immune response to this fungus. The laboratory has made several notable observations that have distinguished the interaction of this intracellular pathogen from that of other microbes. Moreover, some of these finding can be linked to the clinical spectrum, especially our observations regarding the role of tumor necrosis factor-a. Other contributions include the study of the role of regulatory T cells and histoplasmosis, the role chemokines in this disease, and the study of metal regulation by colony stimulating factors. We are exceedingly interested in how zinc regulation dictates the functional attributes of macrophages infected with H. capsulatum. We use a variety of techniques to examine the role of zinc. We have partnered with the Department of Chemistry and bioinformaticians to pursue how zinc and zinc binding proteins shape the biological activity of macrophages. We have extended our work into the examination of transcription factor regulation of macrophages and dendritic cells. For the former hypoxia-inducing factor (HIF) is required for an intact innate immune response to challenge with this organism. We have demonstrated that the absence of HIF-1a in macrophages causes collapse of the immune system. This detrimental effect is caused by elevated interleukin-10 production.
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biorxiv(2023)
Clinical Infectious Diseasesno. 3 (2022): 531-534
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