期刊文献+

高IgE综合征外周血T淋巴细胞亚群和皮肤迟发反应的研究 被引量:2

Analysis of T-lymphocyte subgroups of the peripheral blood and skin DTH in patients with hyper-IgE syndrome
下载PDF
导出
摘要 目的:探讨高IgE综合征病人的细胞免疫功能。方法:分别检测5例高IgE综合征病人和15例健康人的外周血T淋巴细胞亚群和对破伤风类毒素、纯结核菌素的皮肤迟发反应情况。结果:高IgE综合征组外周血CD4+细胞计数比健康对照组显著低(P<0.01),而CD8+细胞计数则比健康对照组高(P<0.01);高IgE综合征病人皮肤迟发反应试验的硬结直径显著小于健康对照组(P<0.01)。结论:高IgE综合征存在T淋巴细胞免疫缺陷,且T淋巴细胞在本病的发病过程中起重要作用。 Objective: To study the function of cellular immunity of patients with hyper-IgE syndrome (HIE). Methods: T-lymphocyte subgroups of the peripheral blood and cutaneous delayed-type hypersensitivity (DTH) to two recall antigens: tetanus toxoid (TT) and purified protein derivative(PPD) were measured in 5 patients with HIE and 15 healthy controls, respectively. Results: The CD4 + cells counted in the HIE group were significantly lower than those in the control group (P<0.01). In contrast, CD8 + cells were significantly higher than those in the controls. The induration sizes induced by DTH to two recall antigens were smaller in HIE patients than those in controls (P<0.01). Conclusion: There is immunological dysfunction of T lymphocyte in the patients with HIE and T cells play an important role in the pathogenesis of HIE.
出处 《中国麻风皮肤病杂志》 2005年第5期333-335,共3页 China Journal of Leprosy and Skin Diseases
关键词 高IGE综合征 外周血 T淋巴细胞亚群 皮肤迟发反应 免疫功能 hyper-IgE syndrome T-lymphocyte subgroups delayed-type hypersensitivity
  • 相关文献

参考文献12

  • 1郑素华,端木宏瑾,李拯民,冯惠忠,张福杰,崔为国,陈明朝,余为业,朱林,谭爱军.人类免疫缺陷病毒(HIV)感染者结核菌素试验反应的研究[J].中国防痨杂志,2002,24(6):320-323. 被引量:19
  • 2Chamlin SL, McCalmont TH, Cunningham BB, el al. Cutaneous manifestations of hyper - IgE syndrome in infants and children. J Pediatr 2002; 141:572.
  • 3Shemer A, Weiss G, Confino Y, et al. The hyper- IgE syndrome.Two cases and review of the literature. Int J Dermatol 2001 ; 40:622.
  • 4Wolach B, Eliakim A, Pomeranz A, el al. Cyclosporin treatment of hyperimmunoglobulin E syndrome, Lancet 1996; 347 : 67.
  • 5Chehimi J, Ehter M, Greene J, el al. Cytokine and chemokine dysregulation in hyper- IgE syndrome. Clin Immunol 2001 ; 100:49.
  • 6King CL, Gallin Jl, Malech HL, et al. Regulation of immunoglobu-lin production in hyperimmunoglobulin E recurrent - infection syndrome by interferon γ. Proc Natl Acad Sci USA 1989;86: 10085.
  • 7Stallone DD, Stunkard AJ, Zweiman B, et al. Decline in delayed-type hypersensitivity response in obese women following weight reduction. Clin Diagn Lab Immunol 1994;1:202.
  • 8Buekley RH, Wray BB, Belmaker EZ. Extreme hyperimmunoglobulinemia E and undue susceptibility to infection. Pediatrics 1972;49:59.
  • 9Del Prete G, Tiri A, Maggi E, et al. Defective in vitro prtxtuctionof gamma - interferon and ttnnor necrosis factor - alpha by circulating T Cells from patients with the hyper- immunoglobulin E syndrome. J Clin Invest 1989;84: 1830.
  • 10Jemec GBE, Heidenheim M. Treatment of hyper - IgE dermatitis with interferon -γ. J Eur Acad Dermatol Venereol 1996 ; 7 : 30.

二级参考文献3

共引文献18

同被引文献13

  • 1Davis SD, Schaller J, Wedgwood RJ. Job's Syndrome. Recurrent,"cold", staphylococcal abscesses[J]. Lancet, 1966, 1(7445): 1013- 1015.
  • 2Chamlin SL, McCalmont TH, Cunningham BB, et al. Cutaneous manifestations of hyper-IgE syndrome in infants and children [J]. J Pediatr, 2002, 141(4): 572-575.
  • 3Grimbacher B, Holland SM, Gallin JI, et al. Hyper-IgE syndrome with recurrent infections-an autosomal dominant multisystem Disorder[J]. N Engl J Med, 1999, 340(9): 692-702.
  • 4Renner ED, Puck JM, Holland SM, et al. Autosomal recessive hyperimmunoglobulin E syndrome: a distinct disease entity[J]. J Pediatr, 2004, 144(1): 93-99.
  • 5Minegishi Y. Hyper-lgE syndrome. Cun" Opin Immunol, 2009,21 ( 5 ): 487-492.
  • 6Holland SM, DeLeo FR, Elloumi HZ, et al. STAT3 mutations in the hyper-IgE syndrome. N Eng! J Med, 2007, 357 (16): 1608- 1619.
  • 7Zhang Q, Davis JC, Lamborn IT, et al. Combined immunodeficiency associated with DOCK8 mutations. N Engl J Med, 2009, 361 (21): 2046-2055.
  • 8Xie L, Hu X, Li Y, et al. Hyper-IgE syndrome with STAT3 mutation: a case report in China's Mainland. Clin Dev Immunol, 2010, 2010: 1-5.
  • 9Minegishi Y, Saito M, Tsuchiya S, et al. Dominant-negative mutations in the DNA-binding domain of STAT3 cause hyper-lgE syndrome. Nature, 2007, 448(7157): 1058-1062.
  • 10Woellner C, Gertz EM, Sehaffer AA, et al. Mutations in STAT3 and diagnostic guidelines for hyper-IgE syndrome. J Allergy Clin Immunol, 2010, 125(2): 424-432.

引证文献2

二级引证文献5

相关作者

内容加载中请稍等...

相关机构

内容加载中请稍等...

相关主题

内容加载中请稍等...

浏览历史

内容加载中请稍等...
;
使用帮助 返回顶部