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Dendritic cell NLRC4 regulates influenza A virus–specific CD4+ T cell responses through FasL expression
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Dendritic cell NLRC4 regulates influenza A virus–specific CD4+ T cell responses through FasL expression
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Journal Article
Dendritic cell NLRC4 regulates influenza A virus–specific CD4+ T cell responses through FasL expression
2019
Overview
Influenza A virus (IAV)-specific T cell responses are important correlates of protection during primary and subsequent infections. 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 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 to wild-type 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 novel 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.
Publisher
American Society for Clinical Investigation
Subject
/ Apoptosis Regulatory Proteins - genetics
/ Apoptosis Regulatory Proteins - immunology
/ Calcium-Binding Proteins - genetics
/ Calcium-Binding Proteins - immunology
/ CD4-Positive T-Lymphocytes - immunology
/ CD4-Positive T-Lymphocytes - pathology
/ CD8-Positive T-Lymphocytes - immunology
/ Defects
/ Dendritic Cells - immunology
/ Fas Ligand Protein - genetics
/ Fas Ligand Protein - immunology
/ Gene Expression Regulation - immunology
/ Influenza A virus - immunology
/ Leucine
/ Ligands
/ Lungs
/ Mice
/ Mutation
/ Orthomyxoviridae Infections - immunology
