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Research Article Free access | 10.1172/JCI115410

An activated CD8+ lymphocyte appears in lymph nodes of rhesus monkeys early after infection with simian immunodeficiency virus.

K A Reimann, G B Snyder, L V Chalifoux, B C Waite, M D Miller, H Yamamoto, O Spertini, and N L Letvin

New England Regional Primate Research Center, Harvard Medical School, Southborough, Massachusetts 01772.

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New England Regional Primate Research Center, Harvard Medical School, Southborough, Massachusetts 01772.

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New England Regional Primate Research Center, Harvard Medical School, Southborough, Massachusetts 01772.

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New England Regional Primate Research Center, Harvard Medical School, Southborough, Massachusetts 01772.

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New England Regional Primate Research Center, Harvard Medical School, Southborough, Massachusetts 01772.

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New England Regional Primate Research Center, Harvard Medical School, Southborough, Massachusetts 01772.

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New England Regional Primate Research Center, Harvard Medical School, Southborough, Massachusetts 01772.

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New England Regional Primate Research Center, Harvard Medical School, Southborough, Massachusetts 01772.

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Published October 1, 1991 - More info

Published in Volume 88, Issue 4 on October 1, 1991
J Clin Invest. 1991;88(4):1113–1120. https://doi.org/10.1172/JCI115410.
© 1991 The American Society for Clinical Investigation
Published October 1, 1991 - Version history
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Abstract

Although alterations in T lymphocyte subset distribution and function in the peripheral blood of HIV-infected humans are well defined, the extent to which these reflect changes in other lymphoid compartments is unclear. We have characterized the coincident changes in PBL and lymph nodes (LN)1 after simian immunodeficiency virus of macaques (SIVmac) infection of rhesus monkeys. Whereas no consistent change in CD8+ PBL was noted during the first 60 d after infection, CD8+ lymphocytes increased significantly in number in LN. These CD8+ LN lymphocytes exhibited an increased expression of MHC class II and a decreased expression of leukocyte adhesion molecule-1, suggesting that they were activated, but interestingly did not express CD25 (IL-2 receptor). Moreover, there was no evidence that these CD8+ LN cells were proliferating, suggesting that they had migrated to the LN. These changes in the LN CD8+ lymphocyte population preceded any detectable change in the light microscopic appearance of the LN. When SIVmac-specific effector T cell responses were assessed, the magnitude of virus-specific effector activity was nearly identical in the PBL and LN of each monkey studied. However, the presence of SIVmac-specific effector cells in the LN did not correlate with the presence of CD8+, MHC class II+ cells. These findings suggest that this numerically important CD8+ lymphocyte subpopulation may serve a regulatory function.

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