Dysfunction of simian immunodeficiency virus/simian human immunodeficiency virus-induced IL-2 expression by central memory CD4+ T lymphocytes

被引:24
|
作者
Sun, Y
Schmitz, JE
Acierno, PM
Santra, S
Subbramanian, RA
Barouch, DH
Gorgone, DA
Lifton, MA
Beaudry, KR
Manson, K
Philippon, V
Xu, L
Maecker, HT
Mascola, JR
Panicali, D
Nabel, GJ
Letvin, NL
机构
[1] Harvard Univ, Beth Israel Deaconess Med Ctr, Sch Med, Div Viral Pathogenesis,Dept Med, Boston, MA 02215 USA
[2] Therion Biol, Cambridge, MA 02142 USA
[3] NIAID, Vaccine Res Ctr, NIH, Bethesda, MD 20892 USA
[4] BD Biosci, San Jose, CA 95131 USA
来源
JOURNAL OF IMMUNOLOGY | 2005年 / 174卷 / 08期
关键词
D O I
10.4049/jimmunol.174.8.4753
中图分类号
R392 [医学免疫学]; Q939.91 [免疫学];
学科分类号
100102 ;
摘要
Production of IL-2 and IFN-gamma by CD4(+) T lymphocytes is important for the maintenance of a functional immune system in infected individuals. In the present study, we assessed the cytokine production profiles of functionally distinct subsets of CD4(+) T lymphocytes in rhesus monkeys infected with pathogenic or attenuated SIV/simian human immunodeficiency virus (SHIV) isolates, and these responses were compared with those in vaccinated monkeys that were protected from immunodeficiency following pathogenic SHIV challenge. We observed that preserved central memory CD4(+) T lymphocyte production of SIV/SHIV-induced IL-2 was associated with disease protection following primate lentivirus infection. Persisting clinical protection in vaccinated and challenged monkeys is thus correlated with a preserved capacity of the peripheral blood central memory CD4(+) T cells to express this important immunomodulatory cytokine.
引用
收藏
页码:4753 / 4760
页数:8
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