Expression of costimulatory molecules on peripheral blood lymphocytes of patients with systemic lupus erythematosus

被引:78
作者
Bijl, M
Horst, G
Limburg, PC
Kallenberg, CGM
机构
[1] Univ Groningen Hosp, Dept Internal Med, Div Clin Immunol, NL-9700 RB Groningen, Netherlands
[2] Univ Groningen Hosp, Dept Rheumatol, NL-9700 RB Groningen, Netherlands
关键词
D O I
10.1136/ard.60.5.523
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
Objective-In systemic lupus erythematosus (SLE) autoantibody production is T cell dependent. For a proper T and B cell interaction, signalling of costimulatory molecules on these cells is necessary. The expression of costimulatory molecules on peripheral blood lymphocytes in patients with SLE in conjunction with disease activity was measured to evaluate whether expression of costimulatory molecules in SLE is increased. Methods-Thirteen patients with SLE with active disease, 10 patients with inactive disease, and 14 controls entered the study. In addition, samples from 10 of the 13 patients with active disease could be studied at a moment of inactive disease as well. Isolated peripheral blood lymphocytes were stained for the lymphocyte subset markers CD4, CD8, CD19, their respective activation markers CD25, HLA-DR, CD38, and the costimulatory molecules CD40L, CD28, CD40, CD80, and CD86. Expression was measured by flow cytometry. Results-Peripheral blood lymphocytes of patients with SLE showed signs of increased activation at the moment of active disease. Almost all CD4+ T cells expressed CD28, both in patients and in controls. CD80 expression on CD19+ B cells was low in both groups and did not correlate with disease activity. In contrast, the percentage of CD19+ B cells expressing CD86 was increased in patients with SLE even in patients with inactive disease (p=0.04) and correlated with the SLEDAI score (p=0.0005) ana levels of anti-dsDNA (p=0.006). No changes in CD40 or CD40L expression were found in the patients with SLE. Conclusion-In patients with SLE the expression of CD86 on CD19+ B cells is increased and is associated with disease activity, B cell activation, and levels of anti-dsDNA. The increased CD86 expression will render (autoreactive) B cells more susceptible for T cells. This can facilitate autoantibody production and might be a target for immunosuppressive treatments.
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页码:523 / 526
页数:4
相关论文
共 15 条
[1]   DERIVATION OF THE SLEDAI - A DISEASE-ACTIVITY INDEX FOR LUPUS PATIENTS [J].
BOMBARDIER, C ;
GLADMAN, DD ;
UROWITZ, MB ;
CARON, D ;
CHANG, CH .
ARTHRITIS AND RHEUMATISM, 1992, 35 (06) :630-640
[2]   Hyperexpression of CD40 ligand by B and T cells in human lupus and its role in pathogenic autoantibody production [J].
DesaiMehta, A ;
Lu, LJ ;
RamseyGoldman, R ;
Datta, SK .
JOURNAL OF CLINICAL INVESTIGATION, 1996, 97 (09) :2063-2073
[3]   TREATMENT OF MURINE LUPUS WITH CTLA4IG [J].
FINCK, BK ;
LINSLEY, PS ;
WOFSY, D .
SCIENCE, 1994, 265 (5176) :1225-1227
[4]   Analysis of CD80 and CD86 expression on peripheral blood B lymphocytes reveals increased expression of CD86 in lupus patients [J].
Folzenlogen, D ;
Hofer, MF ;
Leung, DYM ;
Freed, JH ;
Newell, MK .
CLINICAL IMMUNOLOGY AND IMMUNOPATHOLOGY, 1997, 83 (03) :199-204
[5]   IMPAIRMENT OF ANTIGEN-SPECIFIC T-CELL PRIMING IN MICE LACKING CD40 LIGAND [J].
GREWAL, IS ;
XU, JC ;
FLAVELL, RA .
NATURE, 1995, 378 (6557) :617-620
[6]   B7-1 AND B7-2 COSTIMULATORY MOLECULES ACTIVATE DIFFERENTIALLY THE TH1/TH2 DEVELOPMENTAL PATHWAYS - APPLICATION TO AUTOIMMUNE-DISEASE THERAPY [J].
KUCHROO, VK ;
DAS, MP ;
BROWN, JA ;
RANGER, AM ;
ZAMVIL, SS ;
SOBEL, RA ;
WEINER, HL ;
NABAVI, N ;
GLIMCHER, LH .
CELL, 1995, 80 (05) :707-718
[7]  
Liang BL, 1999, J IMMUNOL, V163, P2322
[8]  
MOHAN C, 1995, J IMMUNOL, V154, P1470
[9]  
Peng SL, 1996, J IMMUNOL, V156, P4041
[10]   CD40 LIGATION INDUCES APO-1/FAS EXPRESSION ON HUMAN B-LYMPHOCYTES AND FACILITATES APOPTOSIS THROUGH THE APO-1/FAS PATHWAY [J].
SCHATTNER, EJ ;
ELKON, KB ;
YOO, DH ;
TUMANG, J ;
KRAMMER, PH ;
CROW, MK ;
FRIEDMAN, SM .
JOURNAL OF EXPERIMENTAL MEDICINE, 1995, 182 (05) :1557-1565