HIGH ANTIGEN REACTIVITY IN MONONUCLEAR-CELLS FROM SITES OF CHRONIC INFLAMMATION

被引:55
作者
RES, PCM
TELGT, D
VANLAAR, JM
POOL, MO
BREEDVELD, FC
DEVRIES, RRP
机构
[1] STATE UNIV LEIDEN HOSP, DEPT RHEUMATOL, 2333 AA LEIDEN, NETHERLANDS
[2] FREE UNIV AMSTERDAM HOSP, DEPT INTERNAL MED, AMSTERDAM, NETHERLANDS
关键词
D O I
10.1016/0140-6736(90)93104-W
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
Antigen-specific in-vitro responses of mononuclear cells from synovial fluid and peripheral blood of patients with rheumatoid arthritis were compared with those of mononuclear cells from pleural exudate and peripheral blood of non-rheumatoid-arthritis patients with chronic pleuritis not caused by tuberculosis. The antigens tested were an acetone-precipitable fraction of Mycobacterium tuberculosis (AP-Mt), an Escherichia coli lysate containing the 65 kD heat-shock protein of MbovisBCG (65 kD/Ecoli), the Mbovis heat-shock protein alone (65 kD), and E coli alone. The mean proliferative responses to AP-Mt were higher in synovial-fluid than in peripheral-blood mononuclear cells in rheumatoid arthritis patients (mean [SEM] stimulation index 10·5 [3·1] vs 2·6 [0·9]) and in pleural-exudate than in peripheral-blood mononuclear cells in the pleuritic patients (7·5 [1·7] vs 3·5 [2·0]). The same pattern was seen for the other three antigens. Only 1 of 26 synovial-fluid mononuclear cell samples from rheumatoid arthritis patients showed a positive response (stimulation index 3 or more) to 65 kD compared with 5 of 22 pleural-exudate mononuclear cell samples, so 65 kD seems not to be the major antigen recognised by synovial-fluid T cells in rheumatoid arthritis. Enhanced reactivity against mycobacterial and other bacterial antigens is not restricted to mononuclear cells from chronically inflamed joints but seems to be a common feature of chronic inflammation. © 1990.
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页码:1406 / 1408
页数:3
相关论文
共 19 条
  • [1] CHARACTERIZATION OF THE IL-2-RECEPTOR ON RHEUMATOID-ARTHRITIS SYNOVIAL-FLUID T-CELLS
    DAUPHINEE, MJ
    DANG, H
    FLESCHER, E
    WILSONBURRIS, K
    GALARZA, D
    HEMPEL, K
    TALAL, N
    [J]. JOURNAL OF AUTOIMMUNITY, 1989, 2 (06) : 813 - 824
  • [2] GASTON JSH, 1989, J IMMUNOL, V143, P2494
  • [3] HARDING B, 1986, CLIN EXP IMMUNOL, V63, P594
  • [4] LINES OF LYMPHOCYTES-T INDUCE OR VACCINATE AGAINST AUTOIMMUNE ARTHRITIS
    HOLOSHITZ, J
    NAPARSTEK, Y
    BENNUN, A
    COHEN, IR
    [J]. SCIENCE, 1983, 219 (4580) : 56 - 58
  • [5] HOLOSHITZ J, 1986, LANCET, V2, P305
  • [6] KLUINNELEMANS HC, 1984, J RHEUMATOL, V11, P272
  • [7] MEDIATOR FO CELLULAR IMMUNITY .2. MIGRATION OF IMMUNOLOGICALLY COMMITTED LYMPHOCYTES INTO INFLAMMATORY EXUDATES
    KOSTER, FT
    MCGREGOR, DD
    MACKANESS, GB
    [J]. JOURNAL OF EXPERIMENTAL MEDICINE, 1971, 133 (02) : 400 - +
  • [8] MEDIATOR OF CELLULAR IMMUNITY .3. LYMPHOCYTE TRAFFIC FROM BLOOD INTO INFLAMED PERITONEAL CAVITY
    KOSTER, FT
    MCGREGOR, DD
    [J]. JOURNAL OF EXPERIMENTAL MEDICINE, 1971, 133 (04) : 864 - &
  • [9] LIFE PF, 1990, CLIN EXP IMMUNOL, V79, P189
  • [10] THE PREFERENTIAL ACCUMULATION OF HELPER-INDUCER LYMPHOCYTE-T IN INFLAMMATORY LESIONS - EVIDENCE FOR REGULATION BY SELECTIVE ENDOTHELIAL AND HOMOTYPIC ADHESION
    PITZALIS, C
    KINGSLEY, G
    HASKARD, D
    PANAYI, G
    [J]. EUROPEAN JOURNAL OF IMMUNOLOGY, 1988, 18 (09) : 1397 - 1404