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The Journal of Immunology, Vol 155, Issue 6 2955-2959, Copyright © 1995 by American Association of Immunologists
ARTICLES |
RA Tripp, SR Sarawar and PC Doherty
Department of Immunology, St. Jude Children's Research Hospital, Memphis, TN 38105, USA.
The development of influenza virus-specific CD8+ cytotoxic T lymphocyte precursors (CTLp) is diminished in H-2b mice that are homozygous (-/-) for disruption of the H-2lAb gene. Virus clearance was not obviously delayed when compared with the congenic H-2lAb (+/+) controls, and evidence of CTL activity was apparent for inflammatory cells recovered from the respiratory tract in both cases. However, the virus-specific CTLp that are normally present in the regional lymph nodes and in the infected lung were evidently being consumed at the peak of the host response to give the terminally differentiated CTL effectors. Even so, any exhaustion of the CTLp pool was apparently transitory with this localized infection as, though the frequencies were consistently lower than those found for the (+/+) controls, CTLp could be detected reproducibly in both lymph nodes and spleen through 14 mo after infection. Analysis of cytokine profiles during the acute response showed a substantial defect in the (-/-) mice, indicating that cytokine production is largely dependent on the influenza-specific CD4+ set.
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