z-logo
Premium
Downregulation of CXCR5 in CD27 − B cells of HIV‐1 infected patients
Author(s) -
Chong Yong,
Nabeshima Shigeki,
Furusyo Norihiro,
Murata Masayuki,
Yamaji Kouzaburo,
Hayashi Jun
Publication year - 2004
Publication title -
journal of medical virology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.782
H-Index - 121
eISSN - 1096-9071
pISSN - 0146-6615
DOI - 10.1002/jmv.20099
Subject(s) - cxcr5 , cd38 , downregulation and upregulation , b cell , chemokine receptor , immunology , chemokine , cxcr4 , biology , cxcl13 , interleukin 21 , virology , t cell , antibody , immune system , microbiology and biotechnology , biochemistry , stem cell , cd34 , gene
The CD27 − (naive) B cells of HIV‐1 infected patients have been shown to be increased in frequency and to be activated, as indicated by high CD38 expression on the cell surface. CXCR5, a B cell chemokine receptor, is expressed on circulating CD27 − (naive) B cells and plays a pivotal role in peripheral B cell development. To investigate the effect of HIV‐1 infection on the expression of this chemokine receptor on naive B cells, the expression level of CXCR5 on CD27 − B cells was examined in 19 drug‐naive HIV‐1 infected patients, 27 HAART‐treated patients, and 20 controls. CXCR5 expression on CD27 − B cells was significantly lower in drug‐naive patients than in HAART‐treated patients and controls ( P  < 0.01). CD27 − B cells with high CD38 expression exhibited low CXCR5 expression. The CXCR5 expression level on CD27 − B cells recovered to within the normal range after effective antiretroviral therapy. These findings suggested that HIV‐1 infection induces a remarkable phenotypic alteration of naive B cells and that the activated naive B cells found in HIV‐1 infection downregulate CXCR5 on their surface. Impaired homing of naive B cells may contribute to HIV‐1 induced immunological deficiencies. J. Med. Virol. 73:362–367, 2004. © 2004 Wiley‐Liss, Inc.

This content is not available in your region!

Continue researching here.

Having issues? You can contact us here