Resident CD8+ and Migratory CD103+ Dendritic Cells Control CD8 T Cell Immunity during Acute Influenza Infection

• Published in: PloS one Vol. 8; no. 6; p. e66136
• Main Authors: Waithman, Jason, Zanker, Damien, Xiao, Kun, Oveissi, Sara, Wylie, Ben, Ng, Royce, Tögel, Lars, Chen, Weisan
• Format: Journal Article
• Language: English
• Published: United States Public Library of Science 04.06.2013; Public Library of Science (PLoS)
• Subjects: Acute Disease; Animals; Antigens; Antigens, CD - metabolism; Biology; Cancer; CD103 antigen; CD11b antigen; CD8 antigen; CD8-Positive T-Lymphocytes - immunology; Cell migration; Cell Movement - immunology; Childrens health; Cytotoxicity; Dendritic cells; Dendritic Cells - cytology; Dendritic Cells - immunology; Dendritic Cells - metabolism; Ethics; Female; Humans; Immunity; Infections; Influenza; Influenza A; Influenza A virus - physiology; Integrin alpha Chains - metabolism; Lymph nodes; Lymphatic system; Lymphocytes; Lymphocytes T; Major histocompatibility complex; Medical research; Medicine; Mice; Orthomyxoviridae Infections - immunology; Science; Studies; T cell receptors; Viral infections; Viruses; Australia; Victoria Australia
• ISSN: 1932-6203; 1932-6203
• DOI: 10.1371/journal.pone.0066136

The identification of the specific DC subsets providing a critical role in presenting influenza antigens to naïve T cell precursors remains contentious and under considerable debate. Here we show that CD8(+) T lymphocyte (TCD8+) responses are severely hampered in C57BL/6 mice deficient in the transcription factor Batf3 after intranasal challenge with influenza A virus (IAV). This transcription factor is required for the development of lymph node resident CD8(+) and migratory CD103(+)CD11b(-) DCs and we found both of these subtypes could efficiently stimulate anti-IAV TCD8+. Using a similar ex vivo approach, many publications on this subject matter excluded a role for resident, non-migratory CD8(+) DC. We postulate the differences reported can partially be explained by how DC are phenotyped, namely the use of MHC class II to segregate subtypes. Our results show that resident CD8(+) DC upregulate this marker during IAV infection and we advise against its use when isolating DC subtypes.