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小鼠对卵清蛋白的口服耐受:化学修饰和“生物过滤”抗原的研究

Oral tolerance to ovalbumin in mice: studies of chemically modified and 'biologically filtered' antigen.

作者信息

Bruce M G, Ferguson A

出版信息

Immunology. 1986 Apr;57(4):627-30.

PMID:2420712
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC1453856/
Abstract

Suppression of systemic immunity after the feeding of antigen was investigated in mice by means of serum transfer experiments. Serum collected from mice 1 hr after a single intragastric dose of 25 mg OVA induced suppression of systemic DTH when injected intraperitoneally into recipient mice. This suppression was found to be restricted to the cell-mediated limb of immunity and was antigen-specific. A postulated function of the intestine, conversion of antigen into tolerogenic form by means of intestinal antigen processing, was studied by attempting to mimic intestinal alteration of OVA by chemical modification of the antigen. Parenteral injection of mice with either deaggregated or denatured OVA did not produce the typical pattern of unresponsiveness seen in animals given intestinally processed OVA. Intestinal processing was also shown to be distinct from systemic antigen processing. Mice injected with serum containing systemically 'filtered' OVA did not become tolerant to OVA in the manner of recipients of serum from OVA-fed mice.

摘要

通过血清转移实验在小鼠中研究了喂食抗原后全身免疫的抑制情况。单次胃内给予25mg卵清蛋白(OVA)1小时后从小鼠收集的血清,当腹腔注射到受体小鼠体内时可诱导全身迟发型超敏反应(DTH)的抑制。发现这种抑制仅限于免疫的细胞介导分支,并且具有抗原特异性。通过尝试通过抗原的化学修饰模拟OVA的肠道改变,研究了肠道的一种假定功能,即将抗原转化为致耐受性形式。给小鼠皮下注射解聚或变性的OVA不会产生在给予经肠道处理的OVA的动物中所见的典型无反应模式。肠道处理也显示与全身抗原处理不同。注射含有经全身“过滤”的OVA的血清的小鼠不会像喂食OVA的小鼠血清的受体那样对OVA产生耐受性。

相似文献

1
Oral tolerance to ovalbumin in mice: studies of chemically modified and 'biologically filtered' antigen.小鼠对卵清蛋白的口服耐受:化学修饰和“生物过滤”抗原的研究
Immunology. 1986 Apr;57(4):627-30.
2
Induction of ovalbumin-specific tolerance by oral administration of Lactococcus lactis secreting ovalbumin.通过口服分泌卵清蛋白的乳酸乳球菌诱导卵清蛋白特异性耐受。
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3
Oral tolerance in protein-deprived mice. II. Evidence of normal 'gut processing' of ovalbumin, but suppressor cell deficiency, in deprived mice.蛋白质缺乏小鼠的口服耐受。II. 蛋白质缺乏小鼠中卵清蛋白 “肠道加工” 正常但抑制细胞缺乏的证据。
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The influence of intestinal processing on the immunogenicity and molecular size of absorbed, circulating ovalbumin in mice.肠道处理对小鼠体内吸收的循环卵清蛋白的免疫原性和分子大小的影响。
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5
Induction of immunological tolerance by oral, but not intravenous and intraportal, administration of ovalbumin and the difference between young and old mice.通过口服(而非静脉注射和门静脉注射)卵清蛋白诱导免疫耐受以及幼鼠与老年鼠之间的差异。
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7
Irradiated mice lose the capacity to 'process' fed antigen for systemic tolerance of delayed-type hypersensitivity.受辐照的小鼠丧失了“处理”摄入抗原以实现迟发型超敏反应全身耐受的能力。
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8
Suppression of an established DTH response to ovalbumin in mice by feeding antigen after immunization.免疫后通过喂食抗原抑制小鼠对卵清蛋白已建立的迟发型超敏反应。
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9
Importance of gastrointestinal ingestion and macromolecular antigens in the vein for oral tolerance induction.胃肠道摄入和静脉内大分子抗原在诱导口服耐受中的重要性。
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10
A genetically determined lack of oral tolerance to ovalbumin is due to failure of the immune system to respond to intestinally derived tolerogen.对卵清蛋白的口腔耐受性在基因上的缺失,是由于免疫系统未能对肠道来源的耐受原作出反应所致。
Eur J Immunol. 1987 Nov;17(11):1673-6. doi: 10.1002/eji.1830171126.

引用本文的文献

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Microb Cell Fact. 2014 Aug 29;13 Suppl 1(Suppl 1):S11. doi: 10.1186/1475-2859-13-S1-S11.
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Innate profiles of cytokines implicated on oral tolerance correlate with low- or high-suppression of humoral response.先天细胞因子谱与体液反应的低抑制或高抑制相关,这与口服耐受有关。
Immunology. 2010 Jul;130(3):447-57. doi: 10.1111/j.1365-2567.2010.03248.x. Epub 2010 Mar 16.
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Serum-derived exosomes from antigen-fed mice prevent allergic sensitization in a model of allergic asthma.来自喂食抗原小鼠的血清源性外泌体可预防过敏性哮喘模型中的过敏致敏。
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Tolerosome-induced oral tolerance is MHC dependent.耐受性微粒体诱导的口服耐受是依赖主要组织相容性复合体的。
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Oral tolerance, an active immunologic process mediated by multiple mechanisms.口服耐受,一种由多种机制介导的主动免疫过程。
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Tolerance and bystander suppression, with involvement of CD25-positive cells, is induced in rats receiving serum from ovalbumin-fed donors.在接受来自喂食卵清蛋白的供体血清的大鼠中,诱导出了耐受性和旁观者抑制,其中CD25阳性细胞参与其中。
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Immunology. 1999 Aug;97(4):565-72. doi: 10.1046/j.1365-2567.1999.00824.x.
10
Oral tolerance and the treatment of rheumatoid arthritis.口服耐受与类风湿关节炎的治疗
Springer Semin Immunopathol. 1998;20(1-2):289-308. doi: 10.1007/BF00832013.

本文引用的文献

1
PHAGOCYTOSIS OF THE ANTIGEN, A CRUCIAL STEP IN THE INDUCTION OF THE PRIMARY RESPONSE.抗原的吞噬作用,是初次免疫应答诱导过程中的关键步骤。
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Hypersensitivity in the small intestinal mucosa. V. Induction of cell-mediated immunity to a dietary antigen.小肠黏膜中的超敏反应。V. 对饮食抗原的细胞介导免疫的诱导。
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Immunological tolerance of the mouse IgE system: dissociation between T cell tolerance and suppressor cell activity.小鼠IgE系统的免疫耐受性:T细胞耐受性与抑制细胞活性之间的分离。
Eur J Immunol. 1980 Aug;10(8):602-8. doi: 10.1002/eji.1830100806.
4
Immunological responses to fed protein antigens in mice. II. Oral tolerance for CMI is due to activation of cyclophosphamide-sensitive cells by gut-processed antigen.小鼠对摄入蛋白质抗原的免疫反应。II. 细胞介导免疫的口服耐受性归因于肠道处理抗原对环磷酰胺敏感细胞的激活。
Immunology. 1983 Jul;49(3):451-6.
5
Immunological responses to fed protein antigens in mice. I. Reversal of oral tolerance to ovalbumin by cyclophosphamide.小鼠对摄入蛋白质抗原的免疫反应。I. 环磷酰胺逆转对卵清蛋白的口服耐受。
Immunology. 1982 Jan;45(1):105-13.
6
Antigen recognition by T cells and B cells: recognition of cross-reactivity between native and denatured forms of globular antigens.T细胞和B细胞的抗原识别:球状抗原天然形式与变性形式之间交叉反应性的识别。
Clin Immunol Immunopathol. 1980 Mar;15(3):397-408. doi: 10.1016/0090-1229(80)90051-3.
7
Protein uptake by the intestine: evidence for absorption of intact macromolecules.肠道对蛋白质的摄取:完整大分子吸收的证据。
Gastroenterology. 1974 May;66(5):987-92.
8
Studies on the induction of immunologic unresponsiveness. 3. Antigen form and mouse strain variation.免疫无反应性诱导的研究。3. 抗原形式与小鼠品系差异。
J Immunol. 1969 Feb;102(2):389-96.
9
Reaginic antibody formation in the mouse. VI. Suppression of IgE and IgG antibody responses to ovalbumin following the administration of high dose urea-denatured antigen.小鼠体内反应素抗体的形成。VI. 给予高剂量尿素变性抗原后对卵清蛋白的IgE和IgG抗体反应的抑制
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10
Strain differences in ease of tolerance induction to bovine gamma-globulin: dependence on macrophage function.牛γ球蛋白耐受性诱导难易程度的品系差异:对巨噬细胞功能的依赖性。
J Immunol. 1975 Jan;114(1 Pt 2):503-6.