Endogenous IFN-γ facilitates Pneumocystis infection and downregulates carbohydrate receptors in CD4+ T cell-depleted mice.
FEBS Lett
; 598(13): 1633-1643, 2024 Jul.
Article
in En
| MEDLINE
| ID: mdl-38631897
ABSTRACT
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.
Key words
Full text:
1
Collection:
01-internacional
Database:
MEDLINE
Main subject:
Phagocytosis
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CD4-Positive T-Lymphocytes
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Down-Regulation
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Interferon-gamma
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Macrophages, Alveolar
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Receptors, Cell Surface
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Lectins, C-Type
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Mannose Receptor
Limits:
Animals
Language:
En
Journal:
FEBS Lett
Year:
2024
Document type:
Article
Affiliation country: