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在未接受过高效抗逆转录病毒治疗(HAART)的无症状HIV-1感染患者中,耗竭B细胞的出现与免疫监视功能降低有关。

Emergence of exhausted B cells in asymptomatic HIV-1-infected patients naïve for HAART is related to reduced immune surveillance.

作者信息

Fogli Manuela, Torti Carlo, Malacarne Fabio, Fiorentini Simona, Albani Melania, Izzo Ilaria, Giagulli Cinzia, Maggi Fabrizio, Carosi Giampiero, Caruso Arnaldo

机构信息

Section of Microbiology, Department of Experimental and Applied Medicine, University of Brescia, Spedali Civili Square, 25123 Brescia, Italy.

出版信息

Clin Dev Immunol. 2012;2012:829584. doi: 10.1155/2012/829584. Epub 2012 Mar 5.

DOI:10.1155/2012/829584
PMID:22474482
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3303688/
Abstract

Alterations of B cell subpopulations have been described up to date as characterizing advanced stage of HIV-1 infection. However, whether such defects are relevant in subjects with a preserved number of CD4⁺ T cells (>350 cells/μL) is unclear. In a cross-sectional study, we investigated if signs of B cells exhaustion and impaired viral immune surveillance are present in a cohort of 43 asymptomatic HIV-1-infected patients with preserved CD4⁺ T cell counts (>350 cells/μL) and highly active antiretroviral therapy (HAART) untreated. A dramatic expansion of exhausted tissue-like memory B cells (CD10⁻CD21(low)CD27⁻) was observed. B cells alteration was related to an increase in Torque teno virus (TTV) load, used as surrogate marker of immune function. Successfully HAART-treated patients showed normalization of B cell subpopulations frequency and TTV load. These results provide new insights on B cell in HIV-1 infection and show that development of B cell abnormalities precedes CD4⁺ T cell decline.

摘要

迄今为止,B细胞亚群的改变被描述为HIV-1感染晚期的特征。然而,这些缺陷在CD4⁺T细胞数量保持正常(>350个细胞/μL)的受试者中是否相关尚不清楚。在一项横断面研究中,我们调查了43名无症状HIV-1感染患者,他们的CD4⁺T细胞计数保持正常(>350个细胞/μL)且未接受高效抗逆转录病毒治疗(HAART),是否存在B细胞耗竭和病毒免疫监测受损的迹象。我们观察到耗竭的组织样记忆B细胞(CD10⁻CD21(低)CD27⁻)显著扩增。B细胞改变与作为免疫功能替代标志物的细小病毒B19(TTV)载量增加有关。成功接受HAART治疗的患者B细胞亚群频率和TTV载量恢复正常。这些结果为HIV-1感染中的B细胞提供了新的见解,并表明B细胞异常的发展先于CD4⁺T细胞下降。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d6f9/3303688/f945c70310cb/CDI2012-829584.005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d6f9/3303688/ab8a254e1bf2/CDI2012-829584.001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d6f9/3303688/59f183ba4b2e/CDI2012-829584.002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d6f9/3303688/0b011dcdd26c/CDI2012-829584.003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d6f9/3303688/2b190daffd40/CDI2012-829584.004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d6f9/3303688/f945c70310cb/CDI2012-829584.005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d6f9/3303688/ab8a254e1bf2/CDI2012-829584.001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d6f9/3303688/59f183ba4b2e/CDI2012-829584.002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d6f9/3303688/0b011dcdd26c/CDI2012-829584.003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d6f9/3303688/2b190daffd40/CDI2012-829584.004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d6f9/3303688/f945c70310cb/CDI2012-829584.005.jpg

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