## Abstract ## Background Apoptosis is one of the possible explanations for the progressive loss of CD4^+^ T lymphocytes in infection with the human immunodeficiency virus (HIV), which may interfere with cell cycle distribution. This study evaluated the cell cycle of CD4^+^ and CD8^+^ lymphocytes
Downregulation of CXCR5 in CD27− B cells of HIV-1 infected patients
✍ Scribed by Yong Chong; Shigeki Nabeshima; Norihiro Furusyo; Masayuki Murata; Kouzaburo Yamaji; Jun Hayashi
- Publisher
- John Wiley and Sons
- Year
- 2004
- Tongue
- English
- Weight
- 119 KB
- Volume
- 73
- Category
- Article
- ISSN
- 0146-6615
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✦ Synopsis
Abstract
The CD27^−^ (naive) B cells of HIV‐1 infected patients have been shown to be increased in frequency and to be activated, as indicated by high CD38 expression on the cell surface. CXCR5, a B cell chemokine receptor, is expressed on circulating CD27^−^ (naive) B cells and plays a pivotal role in peripheral B cell development. To investigate the effect of HIV‐1 infection on the expression of this chemokine receptor on naive B cells, the expression level of CXCR5 on CD27^−^ B cells was examined in 19 drug‐naive HIV‐1 infected patients, 27 HAART‐treated patients, and 20 controls. CXCR5 expression on CD27^−^ B cells was significantly lower in drug‐naive patients than in HAART‐treated patients and controls (P < 0.01). CD27^−^ B cells with high CD38 expression exhibited low CXCR5 expression. The CXCR5 expression level on CD27^−^ B cells recovered to within the normal range after effective antiretroviral therapy. These findings suggested that HIV‐1 infection induces a remarkable phenotypic alteration of naive B cells and that the activated naive B cells found in HIV‐1 infection downregulate CXCR5 on their surface. Impaired homing of naive B cells may contribute to HIV‐1 induced immunological deficiencies. J. Med. Virol. 73:362–367, 2004. © 2004 Wiley‐Liss, Inc.
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