Comparative loss and maturation of peripheral blood dendritic cell subpopulations in African and non-African HIV-1-infected patients

被引:31
作者
Jones, GJ
Watera, C
Patterson, S
Rutebemberwa, A
Kaleebu, P
Whitworth, JA
Gotch, FM
Gilmour, JW
机构
[1] Univ London Imperial Coll Sci Technol & Med, Dept Immunol, Chelsea & Westminster Hosp, Dept Immunol, London SW10 9NH, England
[2] Uganda Virus Res Inst, MRC Programme AIDS Uganda, Entebbe, Uganda
关键词
African; blood dendritic cell; CD11c; CD86; flow-cytometry; HIV-1; maturation; non-glade B;
D O I
10.1097/00002030-200109070-00008
中图分类号
R392 [医学免疫学]; Q939.91 [免疫学];
学科分类号
100102 ;
摘要
Objectives: To quantify the percentage of the two major subpopulations of blood dendritic cells (DC) in HIV-1-seropositive Ugandan individuals infected with nonclade B viruses and compare this with that seen in clade B HIV-1 infected non-African individuals. DC maturation/activation status was also investigated via the expression of CD86. Methods: The percentage of blood DC was quantified by using flow cytometry. DC were identified as the lineage (CD3, CD14, CD16, CD19, CD20, CD56)-negative, HLA-DR-positive population and the two major subpopulations were differentiated by CD11c expression. Results: The percentage of blood DC was reduced significantly in HIV-1-seropositive African individuals when compared with controls (0.21 and 0.39% respectively). A similar reduction was also seen in non-African patients residing in the UK (0.19% compared with 0.36% for controls). However, there was no selective loss in either CD11c-positive or CD11c-negative subpopulations. The percentage of blood DC expressing CD86 was significantly greater in HIV-1-seropositive individuals when compared with controls and the increased expression was largely confined to CD11c-negative DC. Conclusions: Africans infected with non-Glade B HIV-1 showed similar reductions in the percentage of blood DC to non-Africans infected with clade B viruses. There was no selective loss of either DC subpopulation, suggesting that the ability of DC to acquire and present antigens or to produce interferon-a may both be impaired in HIV-1 infection. (C) 2001 Lippincott Williams & Wilkins.
引用
收藏
页码:1657 / 1663
页数:7
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