TRIM26 alleviates fatal immunopathology by regulating inflammatory neutrophil infiltration during Candida infection

Proinflammatory cytokine CXCL1 CXCL2
DOI: 10.1371/journal.ppat.1011902 Publication Date: 2024-01-02T20:13:52Z
ABSTRACT
Fungal infections have emerged as a major concern among immunocompromised patients, causing approximately 2 million deaths each year worldwide. However, the regulatory mechanisms underlying antifungal immunity remain elusive and require further investigation. The E3 ligase Trim26 belongs to tripartite motif (Trim) protein family, which is involved in various biological processes, including cell proliferation, antiviral innate immunity, inflammatory responses. Herein, we report that exerts protective immune functions after fungal infection. -deficient mice are more susceptible fungemia than their wild-type counterparts. Mechanistically, restricts neutrophils infiltration limits proinflammatory cytokine production, can attenuate kidney load renal damage during Candida Trim26-deficient showed higher expression impaired fungicidal activity. We demonstrated excessive was because of increased production chemokines CXCL1 CXCL2, mainly synthesized macrophages or dendritic cells albicans infections. Together, our study findings unraveled vital role regulating through regulation chemokine candidiasis.
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