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国际皮肤性病学杂志 2005 31 (2): 102-104 ISSN: 2096-5540 CN: 32-1880/R |
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B7-CD28/CTLA-4在银屑病的研究进展 |
李圆圆, 王玉坤 |
山东大学齐鲁医院皮肤科 济南 250012 |
收稿日期 2004-07-13 修回日期 null 网络版发布日期 null |
参考文献 [1] Krueger JG. The immunologic basis for the treatment of psoriasis with new biologic agents. J Am Acad Dermatol, 2002, 46:1-23. [2] Chang TT, Kuchroo VK, Sharpe AH. Role of the B7-CD28/CTLA-4 pathway in autoimmune disease. Curr Dir Autoimmun, 2002,5:113-130. [3] Taylor PA, Lees CJ, Fournier S, et al. B7 expression on T cells down-regulates immune responses through CTLA-4 ligation via T-T interactions. J Immunol, 2004, 172:34-39. [4] Ogawa S, Nitta K, Hara Y, et al. CD28 knockout mice as a useful clue to examine the pathogenesis of chronic graft-versus-host reaction. Kidney Int, 2000, 58:2215-2220. [5] Sharpe AH, Freeman GJ. The B7-CD28 superfamily. Nat Rev Immunol, 2002, 2:116-126. [6] Alegre ML, Frauwirth KA, Thompson CB. T-cell regulation by CD28 and CTLA-4. Nat Rev Immunol, 2001,1:220-228. [7] Yu Y, Tang L, Wang J, et al. Psoriatic lesional keratinocytes promote the maturation of human monocyte-derived Langerhans cells. Dermatology, 2002, 204:94-99. [8] Nickoloff BJ. The immunologic and genetic basis of psoriasis. Arch Dermatol, 1999, 135:1104-1110. [9] Ohki O, Yokozeki H, Katayama I, et al. Functional CD86 (B7-2/B70) is predominantly expressed on Langerhans cells in atopic dermatitis. Br J Dermatol, 1997, 136:838-845. [10] Ferenczi K, Burack L, Pope M, et al. CD69, HLA-DR and the IL-2R identify persistently activated T cells in psoriasis vulgaris lesional skin: blood and skin comparisons by flow cytometry. J Autoimmun, 2000, 14:63-78. [11] Coven TR, Murphy FP, Gilleaudeau P, et al. Trimethylpsoralen bath PUVA is a remittive treatment for psoriasis vulgaris. Evidence that epidermal immunocytes are direct therapeutic targets. Arch Dermatol, 1998, 134:1263-1268. [12] Schempp CM, Dittmar HC, Hummler D,et al. Magnesium ions inhibit the antigen-presenting function of human epidermal Langerhans cells in vivo and in vitro. Involvement of ATPase, HLA-DR, B7 molecules, and cytokines. J Invest Dermatol, 2000, 115:680-686. [13] Lenschow DJ, Zeng Y, Thistlethwaite JR, et al. Long-term survival of xenogeneic pancreatic islet grafts induced by CTLA4lg. Science, 1992, 257:789-792. [14] Najafian N, Sayegh MH. CTLA4-Ig: a novel immunosuppressive agent. Expert Opin Investig Drugs, 2000, 9:2147-2157. [15] Abrams JR, Lebwohl MG, Guzzo CA, et al. CTLA4Ig-mediated blockade of T-cell costimulation in patients with psoriasis vulgaris. J Clin Invest, 1999,103:1243-1252. [16] Abrams JR, Kelley SL, Hayes E, et al. Blockade of T lymphocyte costimulation with cytotoxic T lymphocyte-associated antigen 4-immunoglobulin (CTLA4Ig) reverses the cellular pathology of psoriatic plaques, including the activation of keratinocytes, dendritic cells, and endothelial cells. J Exp Med, 2000, 192:681-694. [17] Davenport CM, McAdams HA, Kou J, et al. Inhibition of pro-inflammatory cytokine generation by CTLA4-Ig in the skin and colon of mice adoptively transplanted with CD45RBhi CD4+ T cells correlates with suppression of psoriasis and colitis. Int Immunopharmacol, 2002, 2:653-672. [18] Schopf RE. IDEC-114 (IDEC). Curr Opin Investig Drugs, 2001, 2:635-638. [19] Gottlieb AB, Lebwohl M, Totoritis MC,et al. Clinical and histologic response to single-dose treatment of moderate to severe psoriasis with an anti-CD80 monoclonal antibody. J Am Acad Dermatol, 2002, 47:692-700. [20] Gottlieb AB, Kang S, Linden KG,et al. Evaluation of safety and clinical activity of multiple doses of the anti-CD80 monoclonal antibody, galiximab, in patients with moderate to severe plaque psoriasis. Clin Immunol, 2004, 111:28-37. |
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