tetano
Editor, Senior Moderator
PLoS One. 2013 Jun 4;8(6):e66136. doi: 10.1371/journal.pone.0066136. Print 2013.
Resident CD8(+) and Migratory CD103(+) Dendritic Cells Control CD8 T Cell Immunity during Acute Influenza Infection.
Waithman J, Zanker D, Xiao K, Oveissi S, Wylie B, Ng R, T?gel L, Chen W.
Source
Telethon Institute for Child Health Research and Centre for Child Health Research, University of Western Australia, Perth, Western Australia, Australia ; Ludwig Institute for Cancer Research (Melbourne-Austin Branch), Melbourne, Victoria, Australia.
Abstract
The identification of the specific DC subsets providing a critical role in presenting influenza antigens to na?ve 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.
PMID:
23750278
[PubMed - in process]
PMCID:
PMC3672151
http://www.ncbi.nlm.nih.gov/pubmed/23750278
Resident CD8(+) and Migratory CD103(+) Dendritic Cells Control CD8 T Cell Immunity during Acute Influenza Infection.
Waithman J, Zanker D, Xiao K, Oveissi S, Wylie B, Ng R, T?gel L, Chen W.
Source
Telethon Institute for Child Health Research and Centre for Child Health Research, University of Western Australia, Perth, Western Australia, Australia ; Ludwig Institute for Cancer Research (Melbourne-Austin Branch), Melbourne, Victoria, Australia.
Abstract
The identification of the specific DC subsets providing a critical role in presenting influenza antigens to na?ve 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.
PMID:
23750278
[PubMed - in process]
PMCID:
PMC3672151
http://www.ncbi.nlm.nih.gov/pubmed/23750278