Jaffe J S, James S P, Mullins G E, Braun-Elwert L, Lubensky I, Metcalfe D D
Mucosal Immunity Section, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, Maryland 20892.
J Clin Immunol. 1994 Sep;14(5):299-309. doi: 10.1007/BF01540983.
Allergic eosinophilic gastroenteritis is characterized by elevated total IgE, specific IgE to food antigens, and eosinophilia of tissue and blood. Because the lymphokines IL-4, IL-5, and gamma-interferon, regulate IgE synthesis, and eosinophilopoiesis in vitro, we examined whether there is an imbalance in their production in allergic eosinophilic gastroenteritis. To explore this hypothesis, three adult patients with allergic eosinophilic gastroenteritis were studied. Flow cytometric studies of peripheral blood mononuclear cells from these patients did not reveal evidence of T cell activation or disturbance of T cell numbers or subsets. T cells were capable of normal mitogenic activation in vitro. IL-4 and IL-5 production were markedly elevated with mitogenic stimulation. Most IL-4 and IL-5 production was by CD4+ T cells. Synthesis of IL-5 by CD4+ T lymphocytes in three patients and CD8+ T lymphocytes in two patients occurred in the absence of mitogen. Mitogen-stimulated GM-CSF and gamma-interferon synthesis by CD4+ T cells was normal. Lymphokine mRNA in total cellular RNA derived from endoscopic biopsies was examined by reverse transcription/polymerase chain reaction. Mucosal biopsies from control subjects and most biopsies from allergic eosinophilic gastroenteritis patients contained less than 10(-8) micrograms IL-5 mRNA/1 microgram total cellular mRNA. gamma-Interferon mRNA was not detected by reverse transcription/polymerase chain reaction in biopsies from patients with allergic eosinophilic gastroenteritis but was present in controls. These lymphokine abnormalities are consistent with the elevated IgE and eosinophilia seen in allergic eosinophilic gastroenteritis and suggest that strategies targeting T lymphocytes may be efficacious in treatment of this disease.
变应性嗜酸性粒细胞性胃肠炎的特征为总IgE、食物抗原特异性IgE升高，以及组织和血液中嗜酸性粒细胞增多。由于淋巴因子IL-4、IL-5和γ干扰素在体外调节IgE合成和嗜酸性粒细胞生成，我们研究了变应性嗜酸性粒细胞性胃肠炎患者这些淋巴因子的产生是否失衡。为探讨这一假说，我们对3例成年变应性嗜酸性粒细胞性胃肠炎患者进行了研究。对这些患者外周血单个核细胞的流式细胞术研究未发现T细胞激活、T细胞数量或亚群紊乱的证据。T细胞在体外能够正常地被促有丝分裂原激活。促有丝分裂原刺激后，IL-4和IL-5的产生显著升高。大部分IL-4和IL-5由CD4⁺T细胞产生。3例患者的CD4⁺T淋巴细胞和2例患者的CD8⁺T淋巴细胞在无促有丝分裂原的情况下合成IL-5。促有丝分裂原刺激后，CD4⁺T细胞合成GM-CSF和γ干扰素正常。通过逆转录/聚合酶链反应检测来自内镜活检组织的总细胞RNA中的淋巴因子mRNA。对照受试者的黏膜活检组织以及大部分变应性嗜酸性粒细胞性胃肠炎患者的活检组织中，IL-5 mRNA含量均低于10⁻⁸μg/1μg总细胞mRNA。逆转录/聚合酶链反应在变应性嗜酸性粒细胞性胃肠炎患者的活检组织中未检测到γ干扰素mRNA，但在对照组织中存在。这些淋巴因子异常与变应性嗜酸性粒细胞性胃肠炎中所见的IgE升高和嗜酸性粒细胞增多一致，提示针对T淋巴细胞的治疗策略可能对该病有效。
