国际皮肤性病学杂志    2005 31 (4): 235-237   ISSN: 2096-5540  CN: 32-1880/R   与系统性硬皮病相关的细胞因子 李晶冰, 崔盘根 中国医学科学院 中国协和医科大学皮肤病研究所, 南京210042 收稿日期 2004-12-16  修回日期 null  网络版发布日期 null 参考文献  [1] Denton CP, Abraham DJ. Transforming growth factor-beta and connective tissue growth factor: key cytokines in scleroderma pathogenesis. Curr Opin Rheumatol, 2001, 13:505-511. [2] Kawakami T, Ihn H, Xu W, et al. Increased expression of TGF-beta receptors by scleroderma fibroblasts: evidence for contribution of autocrine TGF-beta signaling to scleroderma phenotype. J Invest Dermatol, 1998, 110:47-51. [3] Kikuchi K, Kadono T, Ihn H, et al. Growth regulation in scleroderma fibroblasts: increased response to transforming growth factor-beta 1. J Invest Dermatol, 1995, 105:128-132. [4] Abraham DJ, Shiwen X, Black CM, et al. Tumor necrosis factor alpha suppresses the induction of connective tissue growth factor by transforming growth factor-beta in normal and scleroderma fibroblasts.J Biol Chem, 2000, 275:15220-15225. [5] Czuwara-Ladykowska J, Gore EA, Shegogue DA, et al. Differential regulation of transforming growth factor-beta receptors type Ⅰ and Ⅱ by platelet-derived growth factor in human dermal fibroblasts. Br J Dermatol, 2001, 145:569-575. [6] Rajkumar VS, Sundberg C, Abraham DJ, et al. Activation of microvascular pericytes in autoimmune Raynaud's phenomenon and systemic sclerosis. Arthritis Rheum, 1999, 42:930-941. [7] Takeda K, Hatamochi A, Arakawa M, et al. Effects of tumor necrosis factor-alpha on connective tissue metabolism in normal and scleroderma fibroblast cultures. Arch Dermatol Res, 1993, 284:440-444. [8] Hasegawa M, Sato S, Nagaoka T, et al. Serum levels of tumor necrosis factor and interleukin-13 are elevated in patients with localized scleroderma. Dermatology, 2003, 207:141-147. [9] Chizzolini C, Parel Y, De Luca C, et al. Systemic sclerosis Th2 cells inhibit collagen production by dermal fibroblasts via membrane-associated tumor necrosis factor alpha. Arthritis Rheum, 2003,48:2593-2604. [10] Kawaguchi Y, Hara M, Wright TM. Endogenous IL-1alpha from systemic sclerosis fibroblasts induces IL-6 and PDGF-A. J Clin Invest, 1999, 103:1253-1260. [11] Hu B, Wang S, Zhang Y, et al. A nuclear target for interleukin-1 alpha: interaction with the growth suppressor necdin modulates proliferation and collagen expression. Proc Natl Acad Sci U S A, 2003,100:10008-10013. [12] Kadono T, Kikuchi K, Ihn H, et al. Increased production of interleukin 6 and interleukin 8 in scleroderma fibroblasts. J Rheumatol,1998, 25:296-301. [13] Atamas SP, Luzina IG, Dai H, et al. Synergy between CD40 ligation and IL-4 on fibroblast proliferation involves IL-4 receptor signaling. J Immunol, 2002, 168:1139-1145. [14] McGaha TL, Le M, Kodera T, et al. Molecular mechanisms of interleukin-4-induced up-regulation of type Ⅰ collagen gene expression in murine fibroblasts. Arthritis Rheum, 2003,48:2275-2284. [15] Sato S, Hanakawa H, Hasegawa M, et al. Levels ofinterleukin 12, a cytokine of type 1 helper T cells, are elevated in sera from patients with systemic sclerosis. J Rheumatol, 2000, 27:2838-2842. [16] Riccieri V, Rinaldi T, Spadaro A, et al. Interleukin-13 in systemic sclerosis: relationship to nailfold capillaroscopy abnormalities. Clin Rheumatol, 2003, 22:102-106. [17] Kurasawa K, Hirose K, Sano H, et al. Increased interleukin-17production in patients with systemic sclerosis. Arthritis Rheum,2000, 43:2455-2463. [18] Molteni M, Della Bella S, Mascagni B, et al. Increased interferongamma (IFN-gamma) levels produced in vitro by alloactivated T lymphocytes in systemic sclerosis and Raynaud's phenomenon. Clin Exp Immunol, 1999, 116:164-168. [19] Selvi E, Tripodi SA, Catenaccio M, et al. Expression of macrophage migration inhibitory factor in diffuse systemic sclerosis. Ann Rheum Dis, 2003, 62:460-464. [20] Kawaguchi Y, Harigai M, Hara M, et al. Expression of hepatocyte growth factor and its receptor (c-met) in skin fibroblasts from patients with systemic sclerosis. J Rheumatol, 2002, 29:1877-1883. 通讯作者: