HIV-1 induces phenotypic and functional perturbations of B cells in chronically infected individuals

被引:247
作者
Moir, S
Malaspina, A
Ogwaro, KM
Donoghue, ET
Hallahan, CW
Ehler, LA
Liu, SY
Adelsberger, J
Lapointe, R
Hwu, P
Baseler, M
Orenstein, JM
Chun, TW
Mican, JAM
Fauci, AS
机构
[1] NIAID, Immunoregulat Lab, NIH, Bethesda, MD 20892 USA
[2] NCI, Surg Branch, NIH, Bethesda, MD 20892 USA
[3] NCI, Frederick Canc & Dev Ctr, Sci Applicat Int Corp, Frederick, MD 21702 USA
[4] George Washington Univ, Dept Pathol, Washington, DC 20037 USA
关键词
D O I
10.1073/pnas.181347898
中图分类号
O [数理科学和化学]; P [天文学、地球科学]; Q [生物科学]; N [自然科学总论];
学科分类号
07 ; 0710 ; 09 ;
摘要
A number of perturbations of B cells has been described in the setting of HIV infection; however, most remain poorly understood. To directly address the effect of HIV replication on B cell function, we investigated the capacity of B cells isolated from HIV-infected patients to respond to a variety of stimuli before and after reduction of viremia by effective antiretroviral therapy. B cells taken from patients with high levels of plasma viremia were defective in their proliferative responses to various stimuli. Viremia was also associated with the appearance of a subpopulation of B cells that expressed reduced levels of CD21. After fractionation into CD21(high)- and CD21(low)-expressing B cells, the CD21(low) fraction showed dramatically reduced proliferation in response to B cell stimuli and enhanced secretion of immunoglobulins when compared with the CD21(high) fraction. Electron microscopic analysis of each fraction revealed cells with plasmacytoid features in the CD21(low) B cell population but not in the CD21(high) fraction. These results indicate that HIV viremia induces the appearance of a subset of B cells whose function is impaired and which may be responsible for the hypergammaglobulinemia associated with HIV disease.
引用
收藏
页码:10362 / 10367
页数:6
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