SERUM LEVELS OF INTERLEUKIN-1B, TUMOR NECROSIS FACTOR-A AND INTERLEUKIN-2 IN RHEUMATOID-ARTHRITIS - CORRELATION WITH DISEASE-ACTIVITY

被引：59
作者：
ALTOMONTE, L
ZOLI, A
MIRONE, L
SCOLIERI, P
MAGARO, M
机构：
[1] Istituto di Clinica Medica, Universita' Cattolica del Sacro Cuore, Roma, 00168, Largo Gemelli
来源：
CLINICAL RHEUMATOLOGY | 1992年 / 11卷 / 02期
关键词：
RHEUMATOID ARTHRITIS; INTERLEUKIN-1B; TUMOR NECROSIS FACTOR-A; INTERLEUKIN-2;
D O I：
10.1007/BF02207957
中图分类号：
R5 [内科学];
学科分类号：
1002 ; 100201 ;
摘要：
Cytokines are potent immunoregulatory factors and may be directly involved in the disordered immunoregulation found in chronic rheumatic diseases. Interleukin-1b (IL-1b), Interleukin-2 (IL-2) and Tumour Necrosis Factor-a (TNF-a) have been implicated in the pathogenesis of rheumatoid arthritis (RA) as mediators of chronic inflammation. Serum levels of IL-1b and TNF-a measured by radioimmunoassay were significantly higher in patients with RA than in healthy controls of similar sex and age while serum levels of IL-2 were significantly lower in the same patients. Further IL-1b and TNF-a were significantly elevated in RA patients with active disease and IL-2 was significantly reduced when compared with patients with low active disease. Serum IL-1b and TNF-a appear to correlate with systemic inflammation, and systemic features of RA may result from dissemination of cytokines produced in the synovium. The role of IL-2 in RA remains controversial. Reduced levels of IL-2 may be an expression of a deficiency of T-cells to produce IL-2 in the active phases of RA or may be due to a possible absorption of IL-2 by lymphocyte receptors.
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页码：202 / 205
页数：4
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共 36 条
  • [1] Dayer J.M., Demezuk S., Cytokines and other mediators in rheumatoid arthritis, Springer Semin Immunopathol, 7, pp. 387-413, (1984)
  • [2] Lipsky P.E., Davis L.S., Lush J.J., Oppenheimer-Marks N., The role of cytokines in the pathogenesis of rheumatoid arthritis, Springer Semin Immunopathol, 11, pp. 123-162, (1989)
  • [3] Ziff M., Role of cytokines in rheumatoid synovitis, Scand J Rheumathol, 76, pp. 211-215, (1988)
  • [4] Arend W.P., Dayer J.M., Cytokines and cytokine inhibitors or antagonists in rheumatoid arthritis, Arthritis Rheum, 33, pp. 305-315, (1990)
  • [5] Emery P., Williaon D.J., Mac Kay I.R., Role of cytokines in rheumatological inflammation, Concepts in Immunopathology, 4, pp. 1-9, (1987)
  • [6] Last-Barry K., Homon C.A., Faanes R.B., Merluzzi V.J., Synergistic and overlapping activities of tumor necrosis factor alpha and interleukin-1, J Immunol, 111, pp. 527-531, (1988)
  • [7] Gowen M., Wood D.D., Ihrie E.J., McGuire M.K.B., Russel R.G., An interleukin-1 like factor stimulates bone resorption in vitro, Nature, 306, pp. 378-380, (1983)
  • [8] Thoon B.M., Mundy G.R., Chambers T.J., Tumor necrosis factor alpha and beta induce osteoblastic cells to stimulate osteoclast bone resorption, J Immunol, 138, pp. 775-779, (1987)
  • [9] Saklatvala J., Tumor necrosis factor-alpha stimulates resorption and inhibits synthesis of proteoglycan in cartilage, Nature, 322, pp. 547-549, (1986)
  • [10] Brinckerhoff C.E., Guyre P.M., Increased proliferation of human synovial fibroblasts treated with recombinant interferon gamma, J Immunol, 134, pp. 3142-3146, (1985)
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