DENDRITIC CELLS FROM HIV-1-INFECTED INDIVIDUALS SHOW REDUCED CAPACITY TO STIMULATE AUTOLOGOUS T-CELL PROLIFERATION

被引:12
作者
ROBERTS, M
GOMPELS, M
PINCHING, AJ
KNIGHT, SC
机构
[1] ST MARYS HOSP, SCH MED, NORTHWICK PK INST MED RES, ANTIGEN PRESENTAT RES GRP, HARROW HA1 3UJ, MIDDX, ENGLAND
[2] SANDOZ CLIN DEV CTR, CAMBERLEY, SURREY, ENGLAND
[3] NEWCASTLE GEN HOSP, DEPT IMMUNOL, Newcastle Upon Tyne, Tyne & Wear, ENGLAND
[4] ST BARTHOLOMEWS HOSP, COLL MED, DEPT IMMUNOL, LONDON, ENGLAND
基金
英国医学研究理事会;
关键词
AUTOLOGOUS MIXED LEUKOCYTE REACTION; PATHOGENESIS OF HIV-1 INFECTION; ANTIBODY PRODUCTION IN HIV INFECTION; CELL-MEDIATED IMMUNITY IN HIV-1 INFECTION; DENDRITIC CELLS IN HIV-1 INFECTION;
D O I
10.1016/0165-2478(94)00147-2
中图分类号
R392 [医学免疫学]; Q939.91 [免疫学];
学科分类号
100102 ;
摘要
Dendritic cells (DC) exposed for a short period of time (1 day) in vitro to HIV infection caused stimulation of autologous T-cells, but those exposed for a longer period (3 days) before addition to T-cells stimulate little or no proliferation [1]. Since a proportion of DC from patients who are HIV-1 seropositive is infected with HIV-1 [2] we used the same culture system to test the level of ongoing stimulation of autologous T-cells by DC. The DC from patients with HIV-1 infection showed no enhanced stimulation of autologous T-cells; they produced significantly lower levels of proliferation than those induced by DC from normal controls or from high risk seronegative individuals. However, DC stimulated production of antibodies to gp120 and p24 in cultures containing autologous B plus T-cell in the absence of any added exogenous antigens as previously described [3]. DC in asymptomatic individuals thus appear to be fuelling antibody production but not T-cell proliferation. The results suggest that a failure by DC to stimulate T-cell proliferation either to HIV-1 or to other environmental antigens may be involved in the failure of cell-mediated responses in HIV infection.
引用
收藏
页码:39 / 43
页数:5
相关论文
共 19 条
[1]  
ALI A, 1993, CLIN EXP IMMUNOL, V94, P32
[2]  
AMADORI A, 1989, J IMMUNOL, V143, P2146
[3]  
AMADORI A, 1991, IMMUNOL TODAY, V12, P94
[4]   RESTORATION OF HIV-SPECIFIC CELL-MEDIATED IMMUNE-RESPONSES BY INTERLEUKIN-12 IN-VITRO [J].
CLERICI, M ;
LUCEY, DR ;
BERZOFSKY, JA ;
PINTO, LA ;
WYNN, TA ;
BLATT, SP ;
DOLAN, MJ ;
HENDRIX, CW ;
WOLF, SF ;
SHEARER, GM .
SCIENCE, 1993, 262 (5140) :1721-1724
[5]  
CLERICI M, 1991, J IMMUNOL, V146, P2207
[6]   A T(H)1-]T(H)2 SWITCH IS A CRITICAL STEP IN THE ETIOLOGY OF HIV-INFECTION [J].
CLERICI, M ;
SHEARER, GM .
IMMUNOLOGY TODAY, 1993, 14 (03) :107-110
[7]  
GARBRECHT FC, 1987, CLIN EXP IMMUNOL, V67, P245
[8]   DEFICIENT AUTOLOGOUS MIXED LYMPHOCYTE-REACTION IN KAPOSIS SARCOMA ASSOCIATED WITH DEFICIENCY OF LEU-3+ RESPONDER T-CELLS [J].
GUPTA, S ;
SAFAI, B .
JOURNAL OF CLINICAL INVESTIGATION, 1983, 71 (02) :296-300
[9]   DENDRITIC CELLS ARE CRITICAL ACCESSORY CELLS FOR THYMUS-DEPENDENT ANTIBODY-RESPONSES IN MOUSE AND IN MAN [J].
INABA, K ;
STEINMAN, RM ;
VANVOORHIS, WC ;
MURAMATSU, S .
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA-BIOLOGICAL SCIENCES, 1983, 80 (19) :6041-6045
[10]   THE ROLE OF DENDRITIC CELLS IN THE INITIATION OF IMMUNE-RESPONSES TO CONTACT SENSITIZERS .1. INVIVO EXPOSURE TO ANTIGEN [J].
KNIGHT, SC ;
KREJCI, J ;
MALKOVSKY, M ;
COLIZZI, V ;
GAUTAM, A ;
ASHERSON, GL .
CELLULAR IMMUNOLOGY, 1985, 94 (02) :427-434