The role of human T-lymphocyte-monocyte contact in inflammation and tissue destruction

被引：0
作者：
Danielle Burger
Jean-Michel Dayer
机构：
[1] University Hospital,Division of Immunology and Allergy, Clinical Immunology Unit
来源：
Arthritis Research & Therapy | / 4卷
关键词：
cytokines; inflammation; monocytes; rheumatoid arthritis; T lymphocytes;
D O I：
暂无
中图分类号：
学科分类号：
摘要：
Contact-mediated signaling of monocytes by human stimulated T lymphocytes (TL) is a potent proinflammatory mechanism that triggers massive upregulation of the proinflammatory cytokines IL-1 and tumor necrosis factor-α. These two cytokines play an important part in chronic destructive diseases, including rheumatoid arthritis. To date this cell–cell contact appears to be a major endogenous mechanism to display such an activity in monocyte-macrophages. Since TL and monocyte-macrophages play a pivotal part in the pathogenesis of chronic inflammatory diseases, we investigated the possible ligands and counter-ligands involved in this cell–cell interaction. We also characterized an inhibitory molecule interfering in this process, apolipoprotein A-I. This review aims to summarize the state of the art and importance of contact-mediated monocyte activation by stimulated TL in cytokine production in rheumatoid arthritis and mechanisms that might control it.
引用
收藏
相关论文
共 292 条
[1]  
Firestein GS(2002)How important are T cells in chronic rheumatoid synovitis?: II. T cell-independent mechanisms from beginning to end. Arthritis Rheum 46 298-308
[2]  
Zvaifler NJ(1992)IFN-gamma and 1,25(OH)2D3 induce on THP-1 cells distinct patterns of cell surface antigen expression, cytokine production, and responsiveness to contact with activated T cells. J Immunol 149 2040-2046
[3]  
Vey E(1993)Cell surface glycoproteins expressed on activated human T-cells induce production of interleukin-1 beta by monocytic cells: a possible role of CD69. Eur Cytokine Netw 4 15-23
[4]  
Zhang JH(1994)Direct contact between T lymphocytes and monocytes is a major pathway for induction of metalloproteinase expression. J Biol Chem 269 22027-22033
[5]  
Dayer J-M(1995)Contact-dependent stimulation of monocytic cells and neutrophils by stimulated human T-cell clones. Immunology 84 571-576
[6]  
Isler P(1996)Expression and cleavage of tumor necrosis factor-alpha and tumor necrosis factor receptors by human monocytic cell lines upon direct contact with stimulated T cells. Eur J Immunol 26 2404-2409
[7]  
Vey E(1997)Human Th1 cells preferentially induce interleukin (IL)-1 beta while Th2 cells induce IL-1 receptor antagonist production upon cell/ cell contact with monocytes. Eur J Immunol 27 171-177
[8]  
Zhang JH(1997)Direct contact with stimulated T cells induces the expression of IL-1 beta and IL-1 receptor antagonist in human monocytes. Involvement of serine/threonine phosphatases in differential regulation. Cytokine 9 480-487
[9]  
Dayer JM(1997)Cytokine stimulation of T lymphocytes regulates their capacity to induce monocyte production of tumor necrosis factor-alpha, but not interleukin-10: Possible relevance to pathophysiology of rheumatoid arthritis. Eur J Immunol 27 624-632
[10]  
Lacraz S(1997)Interleukin-15 mediates T cell-dependent regulation of tumor necrosis factor-alpha production in rheumatoid arthritis. Nat Med 3 189-195
12345678910