Low interleukin-10 production is associated with diabetes in HIV-infected patients undergoing antiviral therapy

被引:8
|
作者
Trabattoni, Daria
Schenal, Monica
Cesari, Miriam
Castelletti, Eleonora
Pacei, Michela
Goldberg, Billi
Gori, Andrea
Clerici, Mario
机构
[1] Univ Milan, Chair Immunol, DISP LITA Vialba, I-20157 Milan, Italy
[2] Univ Milan, Inst Infect Dis & Trop Med, I-20157 Milan, Italy
[3] Int DNCB Study Grp, San Francisco, CA 94131 USA
关键词
diabetes mellitus; interleukin-10; T lymphocytes; ARV; HIV infection;
D O I
10.1007/s00430-005-0006-6
中图分类号
R392 [医学免疫学]; Q939.91 [免疫学];
学科分类号
100102 ;
摘要
Reduced interleukin-10 (IL-10) production is associated with type 2 diabetes in elderly individuals. Antiviral therapy (ARV)-induced immune modulation results in diminished IL-10 production, and diabetes can be observed in ARV-treated human immunodeficiency virus (HIV)-infected individuals. We analyzed, in a cross-sectional pilot study, HIV-antigen-stimulated IL-10 and tumor necrosis factor alpha (TNF alpha) production, and intracellular concentration (ICC), as well as B7-H1 expression, a marker preferentially presented by IL-10-producing cells, in 20 ARV-treated individuals in whom diabetes did (n = 10; diabetes mellitus, DM) or did not (n = 10; controls) develop. Pre-ARV glucose, cholesterol, and triglycerides levels, duration of HIV infection and of therapy, exposure to protease inhibitors (PI), HIV plasma viremia, CD4 counts, and nadir were similar in DM and control patients. Results showed that: (1) IL-10 production was lower; (2) IL-10 ICC was reduced; (3) B7-H1-expressing CD19+ cells were diminished; and (4) TNFa production and ICC by CD4+ T cells was augmented in DM patients. Development of diabetes in HIV infected, ARV-treated individuals could be a response to therapy. Similar to what is observed in elderly individuals, low IL-10 production is associated with diabetes in antiviral-treated HIV infection. Further studies will be necessary to clarify whether low IL-10 is a risk factor for, or a consequence of, diabetes.
引用
收藏
页码:125 / 132
页数:8
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