期刊
BLOOD
卷 117, 期 22, 页码 5870-5880出版社
AMER SOC HEMATOLOGY
DOI: 10.1182/blood-2010-09-310318
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资金
- Food and Drug Administration
- National Institute of Allergy and Infectious Diseases
- Redes Tematicas de Investigacion en SIDA, Spain [ISCIII RETIC RD06/0006/0021]
- Fondo de Investigaciones Sanitarias, Spain [PS09/00424]
The immunomodulatory receptor CD300a is expressed on human B cells. Naive B cells express very low levels of this receptor, whereas memory B cells and plasmablasts/cells express variable levels of CD300a. Germinal center B cells are negative for CD300a expression. Stimulation of naive B cells via B-cell receptor (BCR) and Toll-like receptor 9, along with T-cell help, failed to up-regulate CD300a cell surface expression despite the increased expression of the memory marker CD27 and the down-regulation of CD305. However, Toll-like receptor 9 stimulation alone significantly increased CD300a expression on memory B cells, whereas interleukin-4 and transforming growth factor-beta 1 act as negative regulators of CD300a expression on memory B cells. Coligation of BCR and CD300a inhibits Ca2+ mobilization and nuclear factor of activated T cell transcriptional activity evoked by BCR ligation alone. Suppression of CD300a expression in primary B cells with siRNA resulted in increased BCR-mediated proliferation, thereby con-firming the inhibitory capacity of CD300a. Finally, we show that CD300a expression levels are significantly down-regulated in the circulating B cells of HIV-infected patients. Altogether, these data demonstrate a novel mechanism for suppressing the activity of B cells and suggest a potential role for CD300a in the B-cell dysfunction observed in HIV-induced immunodeficiency. (Blood. 2011; 117(22): 5870-5880)
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