and Impairments in T Helper Cell and Neutrophil Responses against in Knockout Mice.

is a frequently found fungus in Asia, especially China, and it causes primary cutaneous mucormycosis with a high rate of disfigurement. Caspase recruitment domain-containing protein 9 (Card9) is an essential adaptor molecule downstream of C-type lectin receptors. It mediates the activation of nuclear factor kappa B (NF-κB), regulates T helper 1 (Th1) and Th17 differentiation, and plays an important role in fungal immune surveillance. CARD9 deficiency correlates with the increased susceptibility to many fungal infections, including cutaneous mucormycosis caused by However, the underlying immunological mechanisms were not elucidated. Our study established a murine model of subcutaneous infection, and we isolated immune cells, including bone marrow-derived macrophages, bone marrow-derived dendritic cells, naive T cells, and neutrophils, from wild-type (WT) and knockout ( ) mice to examine the antifungal effect of Card9 on and mice exhibited increased susceptibility to infection. Impaired local cytokine and chemokine production, NF-κB (p65) activation, and Th1/17 cell differentiation and partially impaired neutrophil-dependent antifungal immunity were observed in mice. This work enriches our knowledge of the relationship between CARD9 deficiency and mucormycosis.