期刊
JOURNAL OF IMMUNOLOGY
卷 205, 期 3, 页码 573-578出版社
AMER ASSOC IMMUNOLOGISTS
DOI: 10.4049/jimmunol.2000218
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资金
- National Institutes of Health (NIH), National Institute of Allergy and Infectious Diseases (NIAID) Grants [R01AI089952, R01AI124692]
- NIH NIAID Training Grant [T32AI060546]
Myocytes express low levels of MHC class I (MHC I), perhaps influencing the ability of CD8(+) T cells to efficiently detect and destroy pathogens that invade muscle. Trypanosoma cruzi infects many cell types but preferentially persists in muscle, and we asked if this tissue-dependent persistence was linked to MHC expression. Inducible enhancement of skeletal muscle MHC I in mice during the first 20 d of T. cruzi infection resulted in enhanced CD8-dependent reduction of parasite load. However, continued overexpression of MHC I beyond 30 d ultimately led to a collapse of systemic parasite control associated with immune exhaustion, which was reversible in part by blocking PD-1:PD-L1 interactions. These studies demonstrate a surprisingly strong and systemically dominant effect of skeletal muscle MHC expression on maintaining T cell function and pathogen control and argue that the normally low MHC I expression in skeletal muscle is host protective by allowing for pathogen control while preventing immune exhaustion.
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