| Literature DB >> 16849493 |
Tian Wang1, Yunfei Gao, Eileen Scully, C Todd Davis, John F Anderson, Thomas Welte, Michel Ledizet, Raymond Koski, Joseph A Madri, Alan Barrett, Zhinan Yin, Joseph Craft, Erol Fikrig.
Abstract
West Nile (WN) virus causes fatal meningoencephalitis in laboratory mice, and gammadelta T cells are involved in the protective immune response against viral challenge. We have now examined whether gammadelta T cells contribute to the development of adaptive immune responses that help control WN virus infection. Approximately 15% of TCRdelta(-/-) mice survived primary infection with WN virus compared with 80-85% of the wild-type mice. These mice were more susceptible to secondary challenge with WN virus than the wild-type mice that survived primary challenge with the virus. Depletion of gammadelta T cells in wild-type mice that survived the primary infection, however, does not affect host susceptibility during secondary challenge with WN virus. Furthermore, gammadelta T cells do not influence the development of Ab responses during primary and at the early stages of secondary infection with WN virus. Adoptive transfer of CD8(+) T cells from wild-type mice that survived primary infection with WN virus to naive mice afforded partial protection from lethal infection. In contrast, transfer of CD8(+) T cells from TCRdelta(-/-) mice that survived primary challenge with WN virus failed to alter infection in naive mice. This difference in survival correlated with the numeric and functional reduction of CD8 memory T cells in these mice. These data demonstrate that gammadelta T cells directly link innate and adaptive immunity during WN virus infection.Entities:
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Year: 2006 PMID: 16849493 DOI: 10.4049/jimmunol.177.3.1825
Source DB: PubMed Journal: J Immunol ISSN: 0022-1767 Impact factor: 5.422