Endogenous IFN-γ facilitates Pneumocystis infection and downregulates carbohydrate receptors in CD4 + T cell-depleted mice.

Autor: Wang Y; Department of Infection and Host Defense, Shinshu University School of Medicine, Matsumoto, Japan., Nagase H; Department of Infection and Host Defense, Shinshu University School of Medicine, Matsumoto, Japan., Tagawa YI; Department of Biomolecular Functional Engineering, Graduate School of Bioscience and Engineering, Tokyo Institute of Technology, Yokohama, Japan., Taki S; Department of Molecular and Cellular Immunology, Shinshu University School of Medicine, Matsumoto, Japan., Takamoto M; Department of Infection and Host Defense, Shinshu University School of Medicine, Matsumoto, Japan.; Community Health Care Research Center, Nagano University of Health and Medicine, Japan.
Jazyk: angličtina
Zdroj: FEBS letters [FEBS Lett] 2024 Jul; Vol. 598 (13), pp. 1633-1643. Date of Electronic Publication: 2024 Apr 17.
DOI: 10.1002/1873-3468.14875
Abstrakt: IFN-γ plays a critical role in host defense against intracellular pathogens. IFN-γ is produced in the bronchoalveolar lavage fluid of mice infected with Pneumocystis, but the role of IFN-γ in host defense against Pneumocystis remains controversial. It has been previously reported that although exogenous IFN-γ has beneficial effects on eradication of Pneumocystis, endogenous IFN-γ has a negative impact on innate immunity in immunocompromised hosts. Surprisingly, CD4 + T cell-depleted IFN-γ deficient (GKO) mice exhibit resistance to Pneumocystis. Alveolar macrophages (AM) from GKO mice exhibit higher expression of macrophage mannose receptor (MMR) and Dectin-1. Concomitantly, they exhibited greater ability to phagocytize Pneumocystis, and this activity was suppressed by inhibitors of these receptors. Incubation with IFN-γ resulted in a reduction in both the expression of these receptors on AM and their Pneumocystis-phagocytic activity. These results indicate that endogenous IFN-γ facilitates Pneumocystis to escape from host innate immunity by attenuating the phagocytic activity of AM via downregulation of MMR and Dectin-1.
(© 2024 Federation of European Biochemical Societies.)
Databáze: MEDLINE
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