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婴儿期血液单核细胞产生白细胞介素-2和γ-干扰素与父母过敏皮肤试验及随后特应性疾病发生的关联。

Association of interleukin-2 and interferon-gamma production by blood mononuclear cells in infancy with parental allergy skin tests and with subsequent development of atopy.

作者信息

Martinez F D, Stern D A, Wright A L, Holberg C J, Taussig L M, Halonen M

机构信息

Respiratory Sciences Center (Westend Laboratories), University of Arizona HSC, Tucson 85724, USA.

出版信息

J Allergy Clin Immunol. 1995 Nov;96(5 Pt 1):652-60. doi: 10.1016/s0091-6749(95)70264-4.

DOI:10.1016/s0091-6749(95)70264-4
PMID:7499682
Abstract

The mechanisms regulating the onset of atopic sensitization in human beings are not yet fully clarified. We assessed the capacity of mitogen-stimulated umbilical and peripheral blood mononuclear cells to produce interferon-gamma (IFN-gamma) and interleukin-2 (IL-2) at birth and at 9 months of age in 159 infants. Mononuclear cell production of both IFN-gamma and IL-2 at 9 months, but not at birth, was found to be inversely related to parental immediate skin test reactivity to seven local aeroallergens. Skin test reactivity at the age of 6 years was also inversely related to IFN-gamma and IL-2 production at 9 months of age. However, no relationship was evident between total serum IgE levels at 6 years and production of these cytokines at 9 months. The proportions of circulating lymphocytes and CD4+ or CD8+ cells were also unrelated to skin test reactivity at the age of 6 years. These data suggest that mechanisms regulating skin test reactivity to inhaled allergens may involve deficient IFN-gamma production, deficient IL-2 production, or both during or preceding the time of initial sensitization and that additional mechanisms are involved in regulating total serum IgE level.

摘要

人类特应性致敏反应起始的调控机制尚未完全阐明。我们评估了159名婴儿出生时及9个月大时,丝裂原刺激的脐血和外周血单个核细胞产生γ干扰素(IFN-γ)和白细胞介素-2(IL-2)的能力。结果发现,9个月大时单个核细胞产生IFN-γ和IL-2的能力与父母对七种局部气传变应原的即刻皮肤试验反应性呈负相关,而出生时则无此关系。6岁时的皮肤试验反应性也与9个月大时IFN-γ和IL-2的产生呈负相关。然而,6岁时的总血清IgE水平与9个月大时这些细胞因子的产生之间没有明显关系。循环淋巴细胞以及CD4+或CD8+细胞的比例与6岁时的皮肤试验反应性也无关。这些数据表明,调控对吸入性变应原皮肤试验反应性的机制可能涉及初始致敏期间或之前IFN-γ产生不足、IL-2产生不足或两者皆有,并且存在其他机制参与调控总血清IgE水平。

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