CD27−CD38+ B cells accumulated in early HIV infection exhibit transitional profile and promote HIV disease progression
Summary: Although peripheral B cell dysfunction in early HIV infection is established, how B cell subsets are altered by HIV infection is poorly understood. While investigating B cell subsets among individuals recently infected with HIV, we observe an accumulation of CD27−CD38+ B cells and find that...
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Format: | Article |
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Elsevier
2021-07-01
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Series: | Cell Reports |
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Online Access: | http://www.sciencedirect.com/science/article/pii/S2211124721007208 |
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doaj-7f71f2e7447442f3a58bfcdb1ec38f01 |
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record_format |
Article |
collection |
DOAJ |
language |
English |
format |
Article |
sources |
DOAJ |
author |
Yajing Fu Zining Zhang Zhijun Yang Yongjun Jiang Xiaoxu Han Junjie Xu Zhenxing Chu Haibo Ding Sijia He Hong Shang |
spellingShingle |
Yajing Fu Zining Zhang Zhijun Yang Yongjun Jiang Xiaoxu Han Junjie Xu Zhenxing Chu Haibo Ding Sijia He Hong Shang CD27−CD38+ B cells accumulated in early HIV infection exhibit transitional profile and promote HIV disease progression Cell Reports early HIV infection B cell subset HIV disease progression transitional B cells |
author_facet |
Yajing Fu Zining Zhang Zhijun Yang Yongjun Jiang Xiaoxu Han Junjie Xu Zhenxing Chu Haibo Ding Sijia He Hong Shang |
author_sort |
Yajing Fu |
title |
CD27−CD38+ B cells accumulated in early HIV infection exhibit transitional profile and promote HIV disease progression |
title_short |
CD27−CD38+ B cells accumulated in early HIV infection exhibit transitional profile and promote HIV disease progression |
title_full |
CD27−CD38+ B cells accumulated in early HIV infection exhibit transitional profile and promote HIV disease progression |
title_fullStr |
CD27−CD38+ B cells accumulated in early HIV infection exhibit transitional profile and promote HIV disease progression |
title_full_unstemmed |
CD27−CD38+ B cells accumulated in early HIV infection exhibit transitional profile and promote HIV disease progression |
title_sort |
cd27−cd38+ b cells accumulated in early hiv infection exhibit transitional profile and promote hiv disease progression |
publisher |
Elsevier |
series |
Cell Reports |
issn |
2211-1247 |
publishDate |
2021-07-01 |
description |
Summary: Although peripheral B cell dysfunction in early HIV infection is established, how B cell subsets are altered by HIV infection is poorly understood. While investigating B cell subsets among individuals recently infected with HIV, we observe an accumulation of CD27−CD38+ B cells and find that these cells can directly facilitate HIV infection of primary CD4+ T cells in vitro. Comprehensive analyses of the phenotype, function, and transcriptome of the CD27−CD38+ B cell subset is conducted compared with memory and naive B cells. We find that the CD27−CD38+ B cells exhibit a transitional B cell phenotype and an extremely high turnover rate. Importantly, individuals with higher proportions of CD27−CD38+ B cells during early HIV infection tend to become rapid progressors in the chronic infection stage. In this study, we identify a peripheral transitional B cell subset that accumulates during early HIV infection and may contribute to disease progression. |
topic |
early HIV infection B cell subset HIV disease progression transitional B cells |
url |
http://www.sciencedirect.com/science/article/pii/S2211124721007208 |
work_keys_str_mv |
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1721301892079812608 |
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doaj-7f71f2e7447442f3a58bfcdb1ec38f012021-07-15T04:27:18ZengElsevierCell Reports2211-12472021-07-01362109344CD27−CD38+ B cells accumulated in early HIV infection exhibit transitional profile and promote HIV disease progressionYajing Fu0Zining Zhang1Zhijun Yang2Yongjun Jiang3Xiaoxu Han4Junjie Xu5Zhenxing Chu6Haibo Ding7Sijia He8Hong Shang9NHC Key Laboratory of AIDS Immunology (China Medical University), Department of Laboratory Medicine, The First Affiliated Hospital of China Medical University, Shenyang 110001, China; National Clinical Research Center for Laboratory Medicine, The First Affiliated Hospital of China Medical University, Shenyang 110001, China; Collaborative Innovation Center for Diagnosis and Treatment of Infectious Diseases, 79 Qingchun Street, Hangzhou 310003, ChinaNHC Key Laboratory of AIDS Immunology (China Medical University), Department of Laboratory Medicine, The First Affiliated Hospital of China Medical University, Shenyang 110001, China; National Clinical Research Center for Laboratory Medicine, The First Affiliated Hospital of China Medical University, Shenyang 110001, China; Collaborative Innovation Center for Diagnosis and Treatment of Infectious Diseases, 79 Qingchun Street, Hangzhou 310003, ChinaNational Center for Biodefense and Infectious Diseases, School of Systems Biology, George Mason University, Manassas, VA 20110, USANHC Key Laboratory of AIDS Immunology (China Medical University), Department of Laboratory Medicine, The First Affiliated Hospital of China Medical University, Shenyang 110001, China; National Clinical Research Center for Laboratory Medicine, The First Affiliated Hospital of China Medical University, Shenyang 110001, China; Collaborative Innovation Center for Diagnosis and Treatment of Infectious Diseases, 79 Qingchun Street, Hangzhou 310003, ChinaNHC Key Laboratory of AIDS Immunology (China Medical University), Department of Laboratory Medicine, The First Affiliated Hospital of China Medical University, Shenyang 110001, China; National Clinical Research Center for Laboratory Medicine, The First Affiliated Hospital of China Medical University, Shenyang 110001, China; Collaborative Innovation Center for Diagnosis and Treatment of Infectious Diseases, 79 Qingchun Street, Hangzhou 310003, ChinaNHC Key Laboratory of AIDS Immunology (China Medical University), Department of Laboratory Medicine, The First Affiliated Hospital of China Medical University, Shenyang 110001, China; National Clinical Research Center for Laboratory Medicine, The First Affiliated Hospital of China Medical University, Shenyang 110001, China; Collaborative Innovation Center for Diagnosis and Treatment of Infectious Diseases, 79 Qingchun Street, Hangzhou 310003, ChinaNHC Key Laboratory of AIDS Immunology (China Medical University), Department of Laboratory Medicine, The First Affiliated Hospital of China Medical University, Shenyang 110001, China; National Clinical Research Center for Laboratory Medicine, The First Affiliated Hospital of China Medical University, Shenyang 110001, China; Collaborative Innovation Center for Diagnosis and Treatment of Infectious Diseases, 79 Qingchun Street, Hangzhou 310003, ChinaNHC Key Laboratory of AIDS Immunology (China Medical University), Department of Laboratory Medicine, The First Affiliated Hospital of China Medical University, Shenyang 110001, China; National Clinical Research Center for Laboratory Medicine, The First Affiliated Hospital of China Medical University, Shenyang 110001, China; Collaborative Innovation Center for Diagnosis and Treatment of Infectious Diseases, 79 Qingchun Street, Hangzhou 310003, ChinaNHC Key Laboratory of AIDS Immunology (China Medical University), Department of Laboratory Medicine, The First Affiliated Hospital of China Medical University, Shenyang 110001, China; National Clinical Research Center for Laboratory Medicine, The First Affiliated Hospital of China Medical University, Shenyang 110001, China; Collaborative Innovation Center for Diagnosis and Treatment of Infectious Diseases, 79 Qingchun Street, Hangzhou 310003, ChinaNHC Key Laboratory of AIDS Immunology (China Medical University), Department of Laboratory Medicine, The First Affiliated Hospital of China Medical University, Shenyang 110001, China; National Clinical Research Center for Laboratory Medicine, The First Affiliated Hospital of China Medical University, Shenyang 110001, China; Collaborative Innovation Center for Diagnosis and Treatment of Infectious Diseases, 79 Qingchun Street, Hangzhou 310003, China; Corresponding authorSummary: Although peripheral B cell dysfunction in early HIV infection is established, how B cell subsets are altered by HIV infection is poorly understood. While investigating B cell subsets among individuals recently infected with HIV, we observe an accumulation of CD27−CD38+ B cells and find that these cells can directly facilitate HIV infection of primary CD4+ T cells in vitro. Comprehensive analyses of the phenotype, function, and transcriptome of the CD27−CD38+ B cell subset is conducted compared with memory and naive B cells. We find that the CD27−CD38+ B cells exhibit a transitional B cell phenotype and an extremely high turnover rate. Importantly, individuals with higher proportions of CD27−CD38+ B cells during early HIV infection tend to become rapid progressors in the chronic infection stage. In this study, we identify a peripheral transitional B cell subset that accumulates during early HIV infection and may contribute to disease progression.http://www.sciencedirect.com/science/article/pii/S2211124721007208early HIV infectionB cell subsetHIV disease progressiontransitional B cells |