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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 (T CD8+ ) 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 T CD8+ . 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.

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