Ferreira Manuel A R
Queensland Institute of Medical Research, P.O. Royal Brisbane Hospital, Brisbane 4029, Australia.
Mediators Inflamm. 2003 Oct;12(5):259-67. doi: 10.1080/09629350310001619717.
Allergic inflammatory responses are driven by cells of the immune system that rely on cytokines to regulate the activity of other immune and structural cells.
To review published studies to (1) identify cytokines consistently increased after allergen challenge in atopic patients and (2) investigate temporal variation in cytokine expression.
A PUBMED systematic search was used to extract data from studies involving analysis of cytokine expression in fluids or biopsies following in vivo allergen challenge in atopic patients.
Data were extracted from 82 studies. There were no consistent reports of cytokine protein increase in fluids of patients at 0-1 h after challenge. At 4-12 h, the chemokines eotaxin, macrophage inflammatory protein-1alpha, RANTES (regulated on activation normal T cell expressed and secreted) and interleukin (IL)-8 have all been consistently reported to be up-regulated. At 18-24 h after challenge, the lymphokines IL-4, IL-5 and IL-13, as well as the pro-inflammatory cytokines granulocyte-macrophage colony-stimulating factor, tumour necrosis factor-alpha and IL-6 are consistently increased when compared with the respective control value. There were no reports of up-regulation in interferon-gamma protein and mRNA and in IL-2 mRNA.
The expression of granulocyte-macrophage colony-stimulating factor is consistently increased in tissues at 4-12 h after challenge. The influence of this cytokine on antigen capture and presentation by dendritic cells should be further investigated. Additionally, allergen challenge studies are needed that investigate the expression of macrophage-derived chemokine and thymus-regulated and activation-regulated chemokine in tissues of atopic patients. Blocking the effects of these lymphocyte-specific chemokines might provide new therapeutic approaches for the control of allergic inflammation.
过敏性炎症反应由免疫系统细胞驱动,这些细胞依靠细胞因子来调节其他免疫细胞和结构细胞的活性。
回顾已发表的研究,以(1)确定特应性患者在变应原激发后持续增加的细胞因子,以及(2)研究细胞因子表达的时间变化。
采用PUBMED系统检索,从涉及分析特应性患者体内变应原激发后体液或活检组织中细胞因子表达的研究中提取数据。
从82项研究中提取了数据。在激发后0 - 1小时,患者体液中细胞因子蛋白增加并无一致报道。在4 - 12小时,趋化因子嗜酸性粒细胞趋化因子、巨噬细胞炎性蛋白-1α、调节激活正常T细胞表达和分泌因子(RANTES)以及白细胞介素(IL)-8均持续报道上调。在激发后18 - 24小时,与各自对照值相比,淋巴因子IL-4、IL-5和IL-13以及促炎细胞因子粒细胞-巨噬细胞集落刺激因子、肿瘤坏死因子-α和IL-6持续增加。未发现干扰素-γ蛋白和mRNA以及IL-2 mRNA上调的报道。
激发后4 - 12小时,粒细胞-巨噬细胞集落刺激因子在组织中的表达持续增加。应进一步研究该细胞因子对树突状细胞抗原捕获和呈递的影响。此外,需要进行变应原激发研究,以调查特应性患者组织中巨噬细胞衍生趋化因子、胸腺调节和激活调节趋化因子的表达。阻断这些淋巴细胞特异性趋化因子的作用可能为控制过敏性炎症提供新的治疗方法。