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2
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Murine CTLA4-IgG treatment inhibits airway eosinophilia and hyperresponsiveness and attenuates IgE upregulation in a murine model of allergic asthma.在过敏性哮喘小鼠模型中,鼠源CTLA4-IgG治疗可抑制气道嗜酸性粒细胞增多和高反应性,并减弱IgE上调。
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本文引用的文献

1
Unequal death in T helper cell (Th)1 and Th2 effectors: Th1, but not Th2, effectors undergo rapid Fas/FasL-mediated apoptosis.辅助性T细胞(Th)1和Th2效应细胞的死亡不均等:Th1效应细胞而非Th2效应细胞会经历快速的Fas/FasL介导的凋亡。
J Exp Med. 1997 May 19;185(10):1837-49. doi: 10.1084/jem.185.10.1837.
2
Antigen-specific B cells preferentially induce CD4+ T cells to produce IL-4.抗原特异性B细胞优先诱导CD4+T细胞产生白细胞介素-4。
J Immunol. 1997 May 1;158(9):4171-9.
3
Allergic eosinophil-rich inflammation develops in lungs and airways of B cell-deficient mice.在B细胞缺陷小鼠的肺部和气道中会发生富含嗜酸性粒细胞的过敏性炎症。
J Exp Med. 1997 Mar 3;185(5):885-92. doi: 10.1084/jem.185.5.885.
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In differentiated CD4+ T cells, interleukin 4 production is cytokine-autonomous, whereas interferon gamma production is cytokine-dependent.在分化的CD4+ T细胞中,白细胞介素4的产生是细胞因子自主的,而干扰素γ的产生是细胞因子依赖的。
Proc Natl Acad Sci U S A. 1997 Apr 1;94(7):3189-94. doi: 10.1073/pnas.94.7.3189.
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Development of atopic dermatitis-like skin lesion with IgE hyperproduction in NC/Nga mice.NC/Nga小鼠中特应性皮炎样皮肤病变伴IgE过度产生的发展
Int Immunol. 1997 Mar;9(3):461-6. doi: 10.1093/intimm/9.3.461.
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Multiple pathways for the initiation of T helper 2 (Th2) responses.辅助性T细胞2(Th2)应答起始的多种途径。
J Exp Med. 1997 Feb 3;185(3):373-5. doi: 10.1084/jem.185.3.373.
7
Allergic airway sensitization induces T cell activation but not airway hyperresponsiveness in B cell-deficient mice.变应性气道致敏可诱导B细胞缺陷小鼠的T细胞活化,但不会导致气道高反应性。
Proc Natl Acad Sci U S A. 1997 Feb 18;94(4):1350-5. doi: 10.1073/pnas.94.4.1350.
8
Allergen-induced bronchial hyperreactivity and eosinophilic inflammation occur in the absence of IgE in a mouse model of asthma.在一种哮喘小鼠模型中,变应原诱导的支气管高反应性和嗜酸性粒细胞炎症在无IgE的情况下发生。
Proc Natl Acad Sci U S A. 1997 Feb 18;94(4):1344-9. doi: 10.1073/pnas.94.4.1344.
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Human Th2-like cell clones induce IL-12 production by dendritic cells and may express several cytokine profiles.
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Glutathione-S-transferase induces murine dermatitis that resembles human atopic dermatitis.
Clin Exp Allergy. 1996 Nov;26(11):1329-37.

用蛋白质抗原进行表皮致敏,可使小鼠单次暴露于雾化抗原后诱发局部过敏性皮炎,并对乙酰甲胆碱产生高反应性。

Epicutaneous sensitization with protein antigen induces localized allergic dermatitis and hyperresponsiveness to methacholine after single exposure to aerosolized antigen in mice.

作者信息

Spergel J M, Mizoguchi E, Brewer J P, Martin T R, Bhan A K, Geha R S

机构信息

Division of Immunology, Children's Hospital, Harvard Medical School, Boston, Massachusetts 02115, USA.

出版信息

J Clin Invest. 1998 Apr 15;101(8):1614-22. doi: 10.1172/JCI1647.

DOI:10.1172/JCI1647
PMID:9541491
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC508742/
Abstract

Our understanding of the pathogenesis of atopic dermatitis (AD) and its relationship to asthma remains incomplete. Herein, we describe a murine model of epicutaneous (EC) sensitization to the protein allergen, chicken egg albumin, ovalbumin (OVA), which results in a rise in total and OVA-specific serum IgE and leads to the development of a dermatitis characterized by infiltration of CD3(+) T cells, eosinophils, and neutrophils and by local expression of mRNA for the cytokines IL-4, IL-5, and interferon-gamma. A single exposure of the EC sensitized mice to aerosolized OVA induced eosinophilia in the bronchoalveolar lavage fluid and airway hyperresponsiveness to intravenous methacholine as assessed by measurement of pulmonary dynamic compliance (Cdyn). These results suggest a possible role for EC exposure to antigen in atopic dermatitis and in the development of allergic asthma.

摘要

我们对特应性皮炎(AD)的发病机制及其与哮喘的关系的理解仍不完整。在此,我们描述了一种对蛋白质过敏原鸡卵清蛋白(OVA)进行表皮(EC)致敏的小鼠模型,该模型导致总血清IgE和OVA特异性血清IgE升高,并引发一种皮炎,其特征为CD3(+) T细胞、嗜酸性粒细胞和中性粒细胞浸润,以及细胞因子IL-4、IL-5和干扰素-γ的mRNA在局部表达。通过测量肺动态顺应性(Cdyn)评估,将经EC致敏的小鼠单次暴露于雾化OVA会诱导支气管肺泡灌洗液中的嗜酸性粒细胞增多以及气道对静脉注射乙酰甲胆碱的高反应性。这些结果表明,EC暴露于抗原在特应性皮炎和过敏性哮喘的发展中可能起作用。