Changes in antigen densities on leukocyte subsets correlate with progression of HIV disease

被引:37
作者
Roederer, M
Herzenberg, LA
Herzenberg, LA
机构
[1] Department of Genetics, Stanford University, Stanford
关键词
activation markers; antigen density; CD16; CD62L; surrogate markers;
D O I
10.1093/intimm/8.1.1
中图分类号
R392 [医学免疫学]; Q939.91 [免疫学];
学科分类号
100102 ;
摘要
In a cross-sectional study of 154 HIV-infected and 33 uninfected healthy adults, we show that characteristic changes in the levels of expression of leukocyte surface antigens occur in the HIV-infected individuals, These changes, which collectively occur on virtually every leukocyte subset, are specific: a particular antigen may increase or decrease on one subset of PBMC but remain constant on another, Furthermore, within any particular subset, the levels of one or more antigens may change, while the levels of other surface antigens on the same cells remain constant, Some of these antigen density changes have been noted before, e.g. increased CD20 on B cells, and increased CD38 and HLA-DR on CD8 T cells, However, the multiparameter flow cytometry methodology used here reveals changes in a substantially larger number of surface markers, some of which are restricted to fine subsets of PBMC, such as naive or memory T cell subsets, For many of these antigens, the change in expression correlates with absolute CD4 counts; however, some antigens tend to differ most in individuals with CD4 counts >500/mu l; others differ only in those with counts <100/mu l. The changes in antigen densities we observe on B and T cells are consistent with the observation of a persistent quasi-activated state of these cells in HIV-infected individuals, Similarly, the altered expression of the signal-transducing molecules CD7 and CD16 that we demonstrate for NK cells may correlate with the functional defects previously demonstrated in NK cells. Thus, measurements of antigen densities such as those demonstrated here may provide surrogate markers for the altered functional capacities of PBMC subsets in HIV-infected individuals, and may thereby provide a much simpler assay for immunocompetence than in vitro functional assays.
引用
收藏
页码:1 / 11
页数:11
相关论文
共 40 条
[1]   EXPRESSION OF INTERLEUKIN-2 RECEPTORS BY MONOCYTES FROM PATIENTS WITH ACQUIRED-IMMUNODEFICIENCY-SYNDROME AND INDUCTION OF MONOCYTE INTERLEUKIN-2 RECEPTORS BY HUMAN IMMUNODEFICIENCY VIRUS INVITRO [J].
ALLEN, JB ;
MCCARTNEYFRANCIS, N ;
SMITH, PD ;
SIMON, G ;
GARTNER, S ;
WAHL, LM ;
POPOVIC, M ;
WAHL, SM .
JOURNAL OF CLINICAL INVESTIGATION, 1990, 85 (01) :192-199
[2]   MONOCYTE FUNCTIONAL-STUDIES IN ASYMPTOMATIC, HUMAN IMMUNODEFICIENCY DISEASE VIRUS (HIV)-INFECTED INDIVIDUALS [J].
BRAUN, DP ;
KESSLER, H ;
FALK, L ;
PAUL, D ;
HARRIS, JE ;
BLAAUW, B ;
LANDAY, A .
JOURNAL OF CLINICAL IMMUNOLOGY, 1988, 8 (06) :486-494
[3]  
CAI Q, 1990, J ACQ IMMUN DEF SYND, V3, P669
[4]  
CAPSONI F, 1992, CLIN EXP IMMUNOL, V90, P175
[5]   LEUKOCYTE FUNCTION-ASSOCIATED ANTIGEN-1 EXPRESSION ON PERIPHERAL-BLOOD MONONUCLEAR CELL SUBSETS IN HIV-1 SEROPOSITIVE PATIENTS [J].
DESROCHES, CV ;
RIGAL, D .
CLINICAL IMMUNOLOGY AND IMMUNOPATHOLOGY, 1990, 56 (02) :159-168
[6]   POLYMORPHONUCLEAR NEUTROPHILS FROM HUMAN IMMUNODEFICIENCY VIRUS-INFECTED PATIENTS SHOW ENHANCED ACTIVATION, DIMINISHED FMLP-INDUCED L-SELECTIN SHEDDING, AND AN IMPAIRED OXIDATIVE BURST AFTER CYTOKINE PRIMING [J].
ELBIM, C ;
PREVOT, MH ;
BOUSCARAT, F ;
FRANZINI, E ;
CHOLLETMARTIN, S ;
HAKIM, J ;
GOUGEROTPOCIDALO, MA .
BLOOD, 1994, 84 (08) :2759-2766
[7]   SIGNAL TRANSDUCTION THROUGH CROSS-LINKING CD7 AND IGM-FC RECEPTORS THAT INHIBITS T-CELL PROLIFERATION [J].
EMARA, M ;
CARROLL, RG .
HUMAN IMMUNOLOGY, 1992, 34 (03) :181-195
[8]   CELL-SURFACE DOWN-MODULATION OF CD4 AFTER INFECTION [J].
GELEZIUNAS, R ;
BOUR, S ;
WAINBERG, MA .
FASEB JOURNAL, 1994, 8 (09) :593-600
[9]   T-CELL SUBSET ALTERATIONS IN HIV-INFECTED HOMOSEXUAL MEN - NIAID MULTICENTER AIDS COHORT STUDY [J].
GIORGI, JV ;
DETELS, R .
CLINICAL IMMUNOLOGY AND IMMUNOPATHOLOGY, 1989, 52 (01) :10-18
[10]  
GIORGI JV, 1993, J ACQ IMMUN DEF SYND, V6, P904