| Literature DB >> 6265360 |
R H Neubauer, F E Dunn, H Rabin.
Abstract
We examined the association of Herpesvirus saimiri with lymphocyte subsets and the functional integrity and distribution of these populations in owl monkeys with chronic, disease-free infections, in uninoculated, control animals, and in one monkey with H. saimiri-induced lymphoma. The lymphocyte subpopulations examined included total T cells, T cells with receptors for the Fc portion of immunoglobulin G (the Tgamma cells), T cells lacking this receptor (the Tgamma(-) population), and non-T cells. These studies showed that in chronically infected monkeys, H. saimiri was found in both Tgamma and Tgamma(-) populations and that the relative distribution of lymphocyte subsets was not different than the relative distribution in normal animals. The peripheral blood of the one leukemic animal studied showed an increase in total T cells, and both Tgamma and Tgamma(-) cells were increased in number and contained recoverable H. saimiri. In animals with chronic infections, which previously were thought to be immunologically normal, we showed that the Tgamma cells had lost the ability to respond to phytohemagglutinin. When the level of nonspecific cytotoxic activity was examined, we found that the lymphocytes from infected animals were as active as those from uninfected monkeys and that this activity was maintained at normal levels during disease. In the leukemic blood there was a relative increase in the cytotoxic activity of the Tgamma(-) cells. The Tgamma(-) cells obtained from leukemic blood lacked the ability to respond to phytohemagglutinin and could suppress the phytohemagglutinin response of normal cells. This suppressor cell activity was resistant to 3,000 rads of X irradiation. We also found that cells reactive to H. saimiri antigens could be demonstrated in the lymph nodes but not in the peripheral circulation of the lymphomatous monkey.Entities:
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Year: 1981 PMID: 6265360 PMCID: PMC351504 DOI: 10.1128/iai.32.2.698-706.1981
Source DB: PubMed Journal: Infect Immun ISSN: 0019-9567 Impact factor: 3.441