INHIBITION OF T-CELL RESPONSIVENESS DURING EXPERIMENTAL INFECTIONS WITH TRYPANOSOMA-BRUCEI - ACTIVE INVOLVEMENT OF ENDOGENOUS GAMMA-INTERFERON

被引:39
作者
DARJI, A
SILEGHEM, M
HEREMANS, H
BRYS, L
DEBAETSELIER, P
机构
[1] FREE UNIV BRUSSELS,INST MOLEC BIOL,CELLULAR IMMUNOL LAB,B-1050 BRUSSELS,BELGIUM
[2] CATHOLIC UNIV LEUVEN,REGA INST MED RES,B-3000 LOUVAIN,BELGIUM
[3] INT LAB RES ANIM DIS,NAIROBI,KENYA
关键词
D O I
10.1128/IAI.61.7.3098-3102.1993
中图分类号
R392 [医学免疫学]; Q939.91 [免疫学];
学科分类号
100102 ;
摘要
Lymph node cells (LNC) from mice infected with Trypanosoma brucei contain macrophage-like cells that inhibit interleukin-2 receptor (IL-2R) expression (M. Sileghem, A. Darji, R. Hamers, M. Van De Winkel, and P. De Baetselier, Eur. J. Immunol. 19:829-835, 1989). Evidence that gamma interferon (IFN-gamma) is actively involved in (i) the inhibition of IL-2R expression and (ii) the generation of suppressive cells during infections with T. brucei is presented. First, despite an impaired T-cell mitogenic response, LNC from infected mice are hyperresponsive for IFN-gamma production. Second, addition of neutralizing anti-IFN-gamma antibodies to cocultures of normal LNC and suppressive LNC populations reduces the level of suppression and restores the level of IL-2R expression. Third, administration of anti-IFN-gamma to T. brucei-infected animals increases the blastogenic response and reduces the suppressive activity of LNC.
引用
收藏
页码:3098 / 3102
页数:5
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