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| Analysis of B cell phenotype and the restoration of antiretroviral therapy in chronic human immunodeficiency virus type 1 infection |
| YAN Ying-jing1 , QIU Chao1,2,3, LI Liang-Zhu1,2, QIU Chen-Li1, WANG Wan-Hai1, FU Wei-Hui1,2, SUN Jun1, XU Jian-Qing1,2,3, ZHANG Xiao-Yan1,2,3 |
| 1. Shanghai Public Health Clinical Center Affiliated to Fudan University, Shanghai 201508, China; 2. Institutes of Biomedical Sciences, Fudan University, Shanghai 200032, China; 3. Key Laboratory of Medical Molecules Virology of Ministry of Education and Health, Fudan University, Shanghai 200032, China |
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Abstract Human immunodeficiency virus type I （HIV-1） infection leads to severe immune dysfunction. In addition to the progressive depletion and dysfunction of CD4+ T cells, HIV-1 infection also leads to extensive defects in the humoral arm of the immune system. This study aimed to describe the distribution of B cell subpopulations and profiles of activated, apoptosis-associated and costimulatory molecules in each subpopulation. The results showed that the peripheral blood B cell counts in HIV-1 infected patients were significantly lower than that in the healthy controls, but could be restored by antiretroviral therapy (ART). The decline of B cell counts was manifested by the decrease of immature B cells, Naïve B cells, resting memory B cells, and plasmablast. However, tissue-like memory B cells increased significantly. ART could restore the frequencies of naïve B and tissue-like memory B cells, but not the resting memory B cells. CD38 was significantly upregulated in immature B cells, naïve B cells, resting memory B cells and tissue-like memory B cells in HIV-1-infected patients, when compared to healthy controls. All subpopulations showed higher expression of CD95, and naïve B cells, tissue-like memory B cells and plasmablasts exhibited decreased levels of Bcl-2. PD-1 was elevated only in the resting memory cells and plasmablasts. The mean fluorescent intensity of CD40 was diminished in all B cell subpopulations, whereas CD70 decreased in all subpopulations except immature B cells. However, ART could only partially restore the altered expression of the mentioned molecules. These results suggest that HIV-1 infection leads to perturbation of B cell subpopulations, and B cell subpopulations display hyperactivation, susceptibility to apoptosis and impaired interaction with T cells. These alterations could only be restored partially by successful ART, therefore, effective immune intervention strategies should be required.
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Received: 26 July 2013
Published: 01 January 2013
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Corresponding Authors:
ZHANG Xiao-Yan
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