Resident CD8(+) and migratory CD103(+) dendritic cells control CD8 T cell immunity during acute influenza infection

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 transc...

Full description

Saved in:
Bibliographic Details
Published in:PloS one 2013-06, Vol.8 (6), p.e66136-e66136
Main Authors: Waithman, Jason, Zanker, Damien, Xiao, Kun, Oveissi, Sara, Wylie, Ben, Ng, Royce, Tögel, Lars, Chen, Weisan
Format: Article
Language:English
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
Citations: Items that this one cites
Items that cite this one
Online Access:Get full text
Tags: Add Tag
No Tags, Be the first to tag this record!
Description
Summary: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.
ISSN:1932-6203
1932-6203
DOI:10.1371/journal.pone.0066136