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[过敏反应的免疫应答与病理生理学]

[Immune response and pathophysiology of the allergic reaction].

作者信息

Heusser C H, Brinkmann V

机构信息

Pharmazeutische Forschung, Allergie/Immunologie, Ciba-Geigy AG, Basel.

出版信息

Ther Umsch. 1994 Jan;51(1):14-8.

PMID:8146808
Abstract

The allergic immune response is characterized by a number of cellular and molecular interactions. Allergens are taken up through the respiratory or digestion tract or the skin by dendritic cells, B cells or macrophages. After phagocytoses and processing, fragments of allergens are presented to the allergen-specific T cells. By this process, allergen-reactive T cells are induced, which are predominantly of the Th2 type and which secrete the cytokines IL-4, IL-5 and IL-10. In contrast, during a normal immune response to bacterial or viral allergens, T cells of the Th1 type are induced, which produce IFN gamma and IL-2 but not Th2 cytokines. A direct contact of Th2 cells with B cells results in activation of B cells. The Th2 cytokine IL-4 instructs B cells to switch from IgM to IgE antibody production. IgE antibodies play a central role in the induction of allergic diseases. IgE antibodies are taken up by basophils and mast cells by virtue of high-affinity receptors for IgE on these cells. Allergen confrontation leads to the activation of such IgE-sensitized cells, which results in the release of various mediators such as histamine, leukotrienes and prostaglandins; together, they induce the clinical manifestations of allergic reactions. Recent findings have shown that mast cells (and basophils) from atopic tissue are able to produce cytokines such as IL-4 and can thereby induce IgE antibody production. IL-5 generated by allergen-reactive Th2 cells attracts and activates eosinophils, which are responsible for tissue destruction in allergic asthma.(ABSTRACT TRUNCATED AT 250 WORDS)

摘要

过敏免疫反应的特征是一系列细胞和分子相互作用。变应原通过呼吸道或消化道或经皮肤被树突状细胞、B细胞或巨噬细胞摄取。在吞噬和处理后,变应原片段呈递给变应原特异性T细胞。通过这个过程,诱导出变应原反应性T细胞,它们主要是Th2型,并分泌细胞因子IL-4、IL-5和IL-10。相比之下,在对细菌或病毒变应原的正常免疫反应中,诱导出的是Th1型T细胞,它们产生IFNγ和IL-2,但不产生Th2细胞因子。Th2细胞与B细胞的直接接触导致B细胞活化。Th2细胞因子IL-4指导B细胞从产生IgM转换为产生IgE抗体。IgE抗体在过敏性疾病的诱发中起核心作用。IgE抗体凭借这些细胞上的IgE高亲和力受体被嗜碱性粒细胞和肥大细胞摄取。变应原接触导致此类IgE致敏细胞活化,从而释放组胺、白三烯和前列腺素等多种介质;它们共同诱发过敏反应的临床表现。最近的研究结果表明,来自特应性组织的肥大细胞(和嗜碱性粒细胞)能够产生IL-4等细胞因子,从而诱导IgE抗体产生。变应原反应性Th2细胞产生的IL-5吸引并激活嗜酸性粒细胞,嗜酸性粒细胞在过敏性哮喘中导致组织破坏。(摘要截选至250词)

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