Expanded CD4(+)CD45RO(+) phenotype and defective proliferative response in T lymphocytes from patients with Crohn's disease

被引:54
作者
Roman, LI
Manzano, L
DelaHera, A
Abreu, L
Rossi, I
AlvarezMon, M
机构
[1] UNIV ALCALA DE HENARES, PRINCIPE ASTURIAS HOSP, DEPT MED, MADRID, SPAIN
[2] CSIC, CTR INVEST BIOL, MADRID, SPAIN
[3] UNIV AUTONOMA MADRID, DEPT GASTROENTEROL, PUERTA HIERRO HOSP, MADRID, SPAIN
关键词
D O I
10.1053/gast.1996.v110.pm8612987
中图分类号
R57 [消化系及腹部疾病];
学科分类号
摘要
Background & Aims: An abnormal immune response may play a pathogenic role in Crohn's disease, The aim of this study was to determine the role of regulatory T cells in Crohn's disease. Methods: T-cell phenotype and function were studied in blood lymphocytes from patients with Crohn's disease and a control group consisting of healthy donors and patients with ulcerative colitis, Results: Flow cytometric studies showed a significant increase in the percentage of CD3(+)DR(+) and CD4(+)CD45RO(+) T cells in patients with Crohn's disease, T cells from patients with Crohn's disease and ulcerative colitis showed a defective proliferative response after stimulation with surface mitogenic ligands (phytohemagglutinin and anti-CD28 or anti-CD3 antibodies), Soluble interleukin-2 receptor alpha was augmented in the Crohn's disease and ulcerative colitis groups, In the Crohn's disease group, impairment of T-lymphocyte proliferation was normalized by exogenous interleukin 2, although endogenous interleukin-2 production and interleukin-2 receptor a expression were normal, Conclusions: An in vivo expansion of CD4(+) T lymphocytes with memory phenotype and impaired T-cell proliferation that can be restored by pharmacological amounts of interleukin 2 was found in patients with Crohn's disease, There is a severe immunodisturbance in the T-cell compartment of patients with either clinically active or inactive Crohn's disease.
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页码:1008 / 1019
页数:12
相关论文
共 50 条
[1]   STRUCTURE, FUNCTION, AND SEROLOGY OF THE T-CELL ANTIGEN RECEPTOR COMPLEX [J].
ALLISON, JP ;
LANIER, LL .
ANNUAL REVIEW OF IMMUNOLOGY, 1987, 5 :503-540
[2]   CD28 INTERACTION WITH B7-COSTIMULATES PRIMARY ALLOGENEIC PROLIFERATIVE RESPONSES AND CYTOTOXICITY MEDIATED BY SMALL, RESTING LYMPHOCYTES-T [J].
AZUMA, M ;
CAYABYAB, M ;
BUCK, D ;
PHILLIPS, JH ;
LANIER, LL .
JOURNAL OF EXPERIMENTAL MEDICINE, 1992, 175 (02) :353-360
[3]   INOSITOL PHOSPHATES AND CELL SIGNALING [J].
BERRIDGE, MJ ;
IRVINE, RF .
NATURE, 1989, 341 (6239) :197-205
[4]  
BEST WR, 1979, GASTROENTEROLOGY, V77, P843
[5]   AN IMMUNODEFICIENCY CHARACTERIZED BY DEFECTIVE SIGNAL TRANSDUCTION IN LYMPHOCYTES-T [J].
CHATILA, T ;
WONG, R ;
YOUNG, M ;
MILLER, R ;
TERHORST, C ;
GEHA, RS .
NEW ENGLAND JOURNAL OF MEDICINE, 1989, 320 (11) :696-702
[6]   LYMPHOCYTE SUBPOPULATIONS, LYMPHOBLAST TRANSFORMATION ACTIVITY, AND CONCANAVALIN A-INDUCED SUPPRESSOR ACTIVITY IN PATIENTS WITH ULCERATIVE-COLITIS AND CROHNS-DISEASE [J].
DAVIDSEN, B ;
KRISTENSEN, E .
SCANDINAVIAN JOURNAL OF GASTROENTEROLOGY, 1987, 22 (07) :785-790
[7]  
DAVIS L, 1986, J IMMUNOL, V137, P3758
[8]  
DEMON MA, 1986, BLOOD, V67, P228
[9]   PROTEIN-KINASE-C IN T-CELL REGULATION [J].
DROGE, W .
IMMUNOLOGY TODAY, 1986, 7 (11) :340-343
[10]  
FIOCCHI C, 1984, GASTROENTEROLOGY, V86, P734