T cell receptor diversity of CD8+ T lymphocytes and its association with viral load in individuals with HIV-1 infection.
- Author:
Guo-liang REN
1
;
Jian-ping CHEN
;
Ming-ming JIA
;
Zhong-chen KOU
;
Sha LIU
;
Peng-fei MA
;
Yi-ming SHAO
;
Kun-xue HONG
Author Information
- Publication Type:Journal Article
- MeSH: CD8-Positive T-Lymphocytes; immunology; HIV Infections; genetics; virology; HIV-1; immunology; Humans; Polymorphism, Genetic; Receptors, Antigen, T-Cell; genetics; Viral Load
- From: Chinese Journal of Preventive Medicine 2009;43(5):404-408
- CountryChina
- Language:Chinese
-
Abstract:
OBJECTIVETo determine the complementary determining region 3 (CDR3) length diversity of T cell receptor Vbeta repertoires of CD8+ T lymphocytes and to explore its association with viral load in individuals with HIV-1 infection.
METHODSSeparation of CD8+ T cells from peripheral blood mononuclear cells (PBMCs) was carried out by using immunomagnetic beads coated with anti-CD8 antibody. Total RNAs from the purified CD8+ T lymphocytes were isolated and used to perform polymerase chain reaction (PCR) amplifications in CDR3 of 22 T cell receptor (TCR) gene families. CDR3 diversity and its association with viral load in individuals with HIV-1 infection were analyzed.
RESULTSAn average diversity for all CDR3 profiles in CD8+ T cells from 9 HIV-infected individuals was significantly different as compared to 7 age-matched healthy donors (P<0.05) with the HIV-infected individuals losing diversity in the CDR3 profiles. There was positive correlation between changes in TCR CDR3 diversity and viral load (r=0.771, P<0.05). The changes in CDR3 length diversity of Vbeta families in HIV-infected individuals, particular in Vbeta2, Vbeta4, Vbeta5, Vbeta17, Vbeta20, Vbeta21, Vbeta23, Vbeta24, were statistically different from the healthy controls.
CONCLUSIONHIV-1 infection might induce the loss of TCR Vbeta repertoire diversity and disrupt the CDR3 distributions within CD8+ T cells. There should be positive correlation between changes in TCR CDR3 diversity and the viral load in HIV-1 infected patients.