Antigen-specific and non-specific CD4 + T cell recruitment and proliferation during influenza infection

To track epitope-specific CD4 + T cells at a single-cell level during influenza infection, the MHC class II-restricted OVA 323–339 epitope was engineered into the neuraminidase stalk of influenza/A/WSN, creating a surrogate viral antigen. The recombinant virus, influenza A/WSN/OVA II, replicated wel...

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Bibliographic Details
Published in:Virology (New York, N.Y.) N.Y.), 2005-09, Vol.340 (2), p.296-306
Main Authors: Chapman, Timothy J., Castrucci, Maria R., Padrick, Ryan C., Bradley, Linda M., Topham, David J.
Format: Article
Language:English
Subjects:
60 APPLIED LIFE SCIENCES
Adoptive Transfer
Amino Acid Sequence
amino acid sequences
Animals
Antigen
ANTIGENS
CD4 + T cell
CD4-positive T-lymphocytes
CD4-Positive T-Lymphocytes - immunology
Cell Line
CELL PROLIFERATION
cell-mediated immunity
Disease Models, Animal
Dogs
human health
INFLUENZA
Influenza A virus
Influenza A virus - isolation & purification
Kidney
LUNGS
Lymphocyte Activation
Mice
Mice, Inbred C57BL
Mice, Transgenic
Molecular Sequence Data
Orthomyxoviridae Infections - immunology
OVA
Ovalbumin - chemistry
Peptide Fragments
viral antigens
Viral Plaque Assay
VIRUSES
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Summary:To track epitope-specific CD4 + T cells at a single-cell level during influenza infection, the MHC class II-restricted OVA 323–339 epitope was engineered into the neuraminidase stalk of influenza/A/WSN, creating a surrogate viral antigen. The recombinant virus, influenza A/WSN/OVA II, replicated well, was cleared normally, and stimulated both wild-type and DO11.10 or OT-II TCR transgenic OVA-specific CD4 + T cells. OVA-specific CD4 T cells proliferated during infection only when the OVA epitope was present. However, previously primed (but not naive) transgenic CD4 + T cells were recruited to the infected lung both in the presence and absence of the OVA 323–339 epitope. These data show that, when primed, CD4 + T cells may traffic to the lung in the absence of antigen, but do not proliferate. These results also document a useful tool for the study of CD4 T cells in influenza infection.
ISSN:0042-6822
1096-0341
DOI:10.1016/j.virol.2005.06.023