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过敏性哮喘患者B细胞上B7.2而非B7.1的上调。

Upregulation of B7.2, but not B7.1, on B cells from patients with allergic asthma.

作者信息

Hofer M F, Jirapongsananuruk O, Trumble A E, Leung D Y

机构信息

Department of Pediatrics, The National Jewish Medical and Research Center, Denver, CO 80206, USA.

出版信息

J Allergy Clin Immunol. 1998 Jan;101(1 Pt 1):96-102. doi: 10.1016/S0091-6749(98)70199-X.

Abstract

BACKGROUND

Allergic asthma is associated with TH2-like cell responses and increased IgE production. Recent studies in mice have suggested that the costimulatory molecule B7.2 (CD86) may influence the development of TH2 cells.

OBJECTIVE

We sought to determine the potential role of B7.2 in patients with asthma.

METHODS

We performed an analysis of B cells from patients with allergic asthma and healthy control subjects for expression of B7.1 and B7.2 on B cells using five-parameter flow cytometry.

RESULTS

We report that atopic patients with asthma who are exposed to allergens have significantly (p < 0.005) higher levels of B7.2 expression on B cells than atopic asthmatic subjects not exposed to allergen in vivo or nonatopic control subjects. In contrast, there were no differences in B7.1 (CD80) expression among the three study subject groups. When peripheral blood mononuclear cells from asthmatic patients or normal control subjects were stimulated with IL-4 or IL-13, the expression of B7.2, but not B7.1, was significantly increased (p < 0.005) on B cells. Interferon-gamma or IL-12 did not affect the expression of either molecule. The functional significance of B7.2 induction by IL-4 in allergic disease was suggested by the increased expression of this molecule on CD23+, but not CD23-, B cells.

CONCLUSION

These results indicate that the same B cell involved in allergen presentation also expresses the costimulatory molecule B7.2 and support the hypothesis that this molecule is an important costimulatory molecule in allergic responses, the expression of which can be modulated by TH2-like cytokines.

摘要

背景

过敏性哮喘与TH2样细胞反应及IgE产生增加有关。最近在小鼠中的研究表明,共刺激分子B7.2(CD86)可能影响TH2细胞的发育。

目的

我们试图确定B7.2在哮喘患者中的潜在作用。

方法

我们使用五参数流式细胞术分析了过敏性哮喘患者和健康对照者的B细胞中B7.1和B7.2在B细胞上的表达。

结果

我们报告,体内暴露于过敏原的特应性哮喘患者B细胞上B7.2表达水平显著高于未在体内暴露于过敏原的特应性哮喘患者或非特应性对照者(p<0.005)。相比之下,三个研究对象组之间B7.1(CD80)表达没有差异。当用IL-4或IL-13刺激哮喘患者或正常对照者的外周血单个核细胞时,B细胞上B7.2的表达显著增加(p<0.005),而B7.1没有增加。干扰素-γ或IL-12不影响这两种分子的表达。IL-4诱导B7.2在过敏性疾病中的功能意义通过该分子在CD23+而非CD23- B细胞上表达增加得到提示。

结论

这些结果表明,参与过敏原呈递的同一B细胞也表达共刺激分子B7.2,并支持该分子是过敏反应中重要共刺激分子的假说,其表达可由TH2样细胞因子调节。

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