期刊
JOURNAL OF CLINICAL INVESTIGATION
卷 129, 期 7, 页码 2888-2897出版社
AMER SOC CLINICAL INVESTIGATION INC
DOI: 10.1172/JCI124937
关键词
-
资金
- NIH [R01 AI118719, R01 AI104706, T32 AI007485]
- Harry J. Lloyd Charitable Trust
Influenza A virus-specific (IAV-specific) T cell responses are important correlates of protection during primary and subsequent infections. The generation and maintenance of robust IAV-specific T cell responses relies on T cell interactions with dendritic cells (DCs). In this study, we explore the role of the nucleotide-binding domain leucine-rich repeat-containing receptor family member NLRC4 in modulating the DC phenotype during IAV infection. Nlrc4(-/-) mice had worsened survival and increased viral titers during infection, normal innate immune cell recruitment, and IAV-specific CD8(+) T cell responses, but severely blunted IAV-specific CD4(+) T cell responses compared with WT mice. The defect in the pulmonary IAV-specific CD4(+) T cell response was not a result of defective priming or migration of these cells in Nlrc4(-/-) mice but was instead due to an increase in FasL(+) DCs, resulting in IAV-specific CD4(+) T cell death. Together, our data support a role for NLRC4 in regulating the phenotype of lung DCs during a respiratory viral infection and thereby influencing the magnitude of protective T cell responses.
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