期刊名称：Proceedings of the National Academy of Sciences
印刷版ISSN：0027-8424
电子版ISSN：1091-6490
出版年度：2001
卷号：98
期号：16
页码：9283-9288
DOI：10.1073/pnas.161298998
语种：English
出版社：The National Academy of Sciences of the United States of America
摘要：The synthesis of antiviral {beta}-chemokines has joined cytolysis as a potential mechanism for the control of HIV-1 infection by CD8+ T cells. Recent evidence suggests that these two effector functions can diverge in some individuals infected with HIV-1; however, little is known about the CD8+ T cell subsets in normal individuals that synthesize antiviral {beta}-chemokines. In this report, we have used mutliparameter flow cytometry to characterize the T cell subsets that secrete the antiviral {beta}-chemokine macrophage inflammatory protein (MIP)-1{beta}. These studies have shown: (i) CD8+ cells are the predominant T cell subset that synthesizes MIP-1{beta}; (ii) MIP-1{beta} and IFN-{gamma} are synthesized congruently in most CD8+ T cells; however, significant numbers of these cells synthesize only one of these effector molecules; (iii) approximately 60% of the CD8+ T cells that synthesize MIP-1{beta} lack perforin; (iv) MIP-1{beta} is synthesized with approximately equal frequency by CD28+ and CD28- subpopulations of CD8+ T cells; (v) MIP-1{beta} is synthesized by three distinct CD8+ T cell subsets defined by the expression of CD45R0 and CD62L; and (vi) MIP-1{beta} is not synthesized in short-term cultures of naive CD8+ T cells. These results demonstrate substantial subset heterogeneity of MIP-1{beta} synthesis among CD8+ T cells and suggest that these subsets should be evaluated as correlates of protective immunity against HIV-1.
