Cutting Edge: Activation of Virus-Specific CD4 T Cells throughout γ-Herpesvirus Latency
Author(s) -
Michael L. Freeman,
Claire E. Burkum,
Kathleen G. Lanzer,
Meghan K. Jensen,
Mushtaq Ahmed,
Eric J. Yager,
Emilio Flaño,
Gary M. Winslow,
David L. Woodland,
Marcia A. Blackman
Publication year - 2011
Publication title -
the journal of immunology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.737
H-Index - 372
eISSN - 1550-6606
pISSN - 0022-1767
DOI - 10.4049/jimmunol.1102745
Subject(s) - biology , epitope , cytotoxic t cell , t cell , latency (audio) , interleukin 21 , cd8 , immune system , mhc class i , microbiology and biotechnology , virology , immunology , antigen , in vitro , genetics , electrical engineering , engineering
CD4 T cells are essential for immune control of γ-herpesvirus latency. We previously identified a murine MHC class II-restricted epitope in γ-herpesvirus-68 gp150 (gp150(67-83)I-A(b)) that elicits CD4 T cells that are maintained throughout long-term infection. However, it is unknown whether naive cells can be recruited into the antiviral CD4 T cell pool during latency. In this study, we generate a mouse transgenic for a gp150-specific TCR and show epitope-specific activation of transgenic CD4 T cells during acute and latent infections. Furthermore, although only dendritic cells can stimulate virus-specific CD8 T cells during latency, we show that both dendritic cells and B cells stimulate transgenic CD4 T cells. These studies demonstrate that naive CD4 T cells specific for a viral glycoprotein can be stimulated throughout infection, even during quiescent latency, suggesting that CD4 T cell memory is maintained in part by the continual recruitment of naive cells.
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