|
国际皮肤性病学杂志 2004 30 (4): 232-234 ISSN: 2096-5540 CN: 32-1880/R |
|
|
|
|
|
变应性接触性皮炎中细胞因子的表达 |
李春联1, 陈德利1, 王学民2 |
1. 同济大学医学院附属同济医院皮肤科, 上海200180; 2. 上海市皮肤病性病医院 |
收稿日期 2003-08-29 修回日期 null 网络版发布日期 null |
参考文献 [1] Grabbe S, Schwarz T. Immunoregulatory mechanisms involved in elicitation of allergic contact hypersensitivity. Immunol Today, 1998, 19:37-44. [2] Cumberbetch M, Dearman RJ, Kimber I. Langerhans cells require signals from both tumour necrosis factor-alpha and interleukin-1 beta for migration. Immunology, 1997,92:388-395. [3] Okazaki F, Kanzaki H, Fujii K, et al. Initial recruitment of interferon-gamma-producing CD8 + effector cells, followed by infiltration of CD4 + cells in 2,4,6-trinitro-1-chlorobenzene (TNCB)-induced murine contact hypersensitivity reactions. J Dermatol, 2002, 29:699. [4] Dearman RJ, Cumberbatch M, Hilton J, et al. A re-appraisal of the skin-sensitizing activity of 2,4-dinitrothiocyanobenzene. Food Chem Toxicol, 1997, 35:261-269. [5] Biedermann T, Mailhammer R, Mai A,et al. Reversal of established delayed type hypersensitivity reactions following therapy with IL-4 or antigen-specific Th2 cells. Eur J Immunol, 2001, 31:1582-1591. [6] Garrigue JL, Nicolas JF, Fraginals R, et al. Optimization of the mouse ear swelling test for in vivo and in vitro studies of weak contact sensitizers. Contact Dermatitis, 1994, 30:231-237. [7] Westphal GA, Schnuch A, Moessner R, et al. Cytokine gene polymorphisms in allergic contact dermatitis. Contact Dermatitis, 2003,48:93-98. [8] Groves RW, Allen MH, Ross EL, et al. Tumour necrosis factor alpha is pro-inflammatory in normal human skin and modulates cutaneous adhesion molecule expression. Br J Dermatol, 1995, 132:345-352. [9] Sheu MY, Fowler AJ, Kao J, et al. Topical peroxisome proliferator activated receptor-alpha activators reduce inflammation in irritant and allergic contact dermatitis models. J Invest Dermatol, 2002, 118:94-101. [10] Pichowski JS, Cumberbatch M, Dearman, et al. Investigation of induced changes in interleukin 1 beta mRNA expression by cultured human dendritic cells as an in vitro approach to skin sensitization testing. Toxicol In Vitro, 2000, 14:351-360. [11] Nishimura N, Tohyama C, Satoh M, et al. Defective immune response and severe skin damage following UVB irradiation in interleukin-6-deficient mice. Immunology, 1999, 97:77-83. [12] Wang B, Zhuang L, Fujisawa H, et al. Enhanced epidermal Langerhans cell migration in IL-10 knockout mice. J Immunol, 1999,162:277-283. [13] Nakae S, Komiyama Y, Nambu A, et al. Antigen-specific T cell sensitization is impaired in IL-17-deficient mice, causing suppression of allergic cellular and humoral responses. Immunity, 2002, 17:375-387. [14] Yawalkar N, Brand CU, Braathen LR. Interleukin-12 expression in human afferent lymph derived from the induction phase of allergic contact dermatitis. Br J Dermatol, 1998, 138:297-300. [15] Albanesi C, Scarponi C, Cavani A, et al. Interleukin-17 is produced by both Thl and Th2 lymphocytes, and modulates interferongamma-and interleukin-4-induced activation of human keratinocytes.J Invest Dermatol, 2000, 115:81-87. [16] Meng X, Sawamura D, Tamai K,et al. Keratinocyte gene therapy for systemic diseases. Circulating interleukin 10 released from gene-transferred keratinocytes inhibits contact hypersensitivity at distant areas of the skin. J Clin Invest, 1998, 101:1462-1467. |
|
|
|
通讯作者: |
|