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1
Lack of oral tolerance in C3H/HeJ mice.C3H/HeJ小鼠中缺乏口服耐受。
J Exp Med. 1982 Feb 1;155(2):605-10. doi: 10.1084/jem.155.2.605.
2
Isotype-specific immunoregulation. Evidence for a distinct subset of T contrasuppressor cells for IgA responses in murine Peyer's patches.同种型特异性免疫调节。小鼠派尔集合淋巴结中存在针对IgA应答的独特T反抑制细胞亚群的证据。
J Exp Med. 1986 Aug 1;164(2):501-16. doi: 10.1084/jem.164.2.501.
3
Murine immune responses to Salmonella lipopolysaccharide: oral administration of whole bacteria to C3H/HeJ mice induces secondary anti-LPS responses, especially of the IgA isotype.小鼠对沙门氏菌脂多糖的免疫反应:给C3H/HeJ小鼠口服完整细菌可诱导继发性抗脂多糖反应,尤其是IgA同种型的反应。
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4
IgA responses in xid mice: oral antigen primes Peyer's patch cells for in vitro immune responses and secretory antibody production.Xid小鼠中的IgA应答:口服抗原使派尔集合淋巴结细胞致敏以产生体外免疫应答和分泌性抗体。
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5
Murine bone marrow IgA responses to orally administered sheep erythrocytes.小鼠骨髓对口服绵羊红细胞的IgA应答。
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6
Mucosal immunoregulation: environmental lipopolysaccharide and GALT T lymphocytes regulate the IgA response.黏膜免疫调节:环境脂多糖和肠道相关淋巴组织T淋巴细胞调节IgA反应。
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In vivo immune response to a T-cell-dependent antigen by cultures of disassociated murine Peyer's patch.用分离的小鼠派尔集合淋巴结培养物对T细胞依赖性抗原的体内免疫反应。
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Contrasuppressor cells that break oral tolerance are antigen-specific T cells distinct from T helper (L3T4+), T suppressor (Lyt-2+), and B cells.破坏口服耐受性的抗抑制细胞是不同于辅助性T细胞(L3T4 +)、抑制性T细胞(Lyt - 2 +)和B细胞的抗原特异性T细胞。
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Functional characteristics of Peyer's patch lymphoid cells. II. Lipopolysaccharide is thymus dependent.派尔集合淋巴结淋巴细胞的功能特性。II. 脂多糖依赖胸腺。
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LPS regulation of the immune response: suppression of immune responses to orally administered T-independent antigen.脂多糖对免疫反应的调节:抑制对口服非胸腺依赖性抗原的免疫反应。
J Immunol. 1981 Sep;127(3):1052-7.

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本文引用的文献

1
Systemic tolerance and secretory immunity after oral immunization.口服免疫后的全身耐受性和分泌性免疫
J Exp Med. 1980 Dec 1;152(6):1459-72. doi: 10.1084/jem.152.6.1459.
2
Immunobiology of dental caries: microbial aspects and local immunity.龋齿的免疫生物学:微生物学方面与局部免疫
Annu Rev Microbiol. 1981;35:595-638. doi: 10.1146/annurev.mi.35.100181.003115.
3
Cellular basis for elevated IgA responses in C3H/HeJ mice.C3H/HeJ小鼠中IgA反应升高的细胞基础。
J Immunol. 1980 Aug;125(2):732-7.
4
Two distinct antigen-specific suppressor factors induced by the oral administration of antigen.经口服抗原诱导产生的两种不同的抗原特异性抑制因子。
J Exp Med. 1980 Sep 1;152(3):545-54. doi: 10.1084/jem.152.3.545.
5
Oral tolerance.口服耐受
Transplantation. 1980 May;29(5):353-6. doi: 10.1097/00007890-198005000-00001.
6
A mechanism for the induction of immunological tolerance by antigen feeding: antigen-antibody complexes.通过抗原喂食诱导免疫耐受的机制:抗原-抗体复合物
J Exp Med. 1975 Dec 1;142(6):1509-19. doi: 10.1084/jem.142.6.1509.
7
The Qa-1 antigenic system. Relation of Qa-1 phenotypes to lymphocyte sets, mitogen responses, and immune functions.Qa-1抗原系统。Qa-1表型与淋巴细胞集落、丝裂原反应及免疫功能的关系。
J Exp Med. 1978 Oct 1;148(4):963-73. doi: 10.1084/jem.148.4.963.
8
Cellular requirements for lipopolysaccharide adjuvanticity. A role for both T lymphocytes and macrophages for in vitro responses to particulate antigens.脂多糖佐剂活性的细胞需求。T淋巴细胞和巨噬细胞在体外对颗粒性抗原应答中的作用。
J Exp Med. 1979 Apr 1;149(4):793-807. doi: 10.1084/jem.149.4.793.
9
Modulation of immune response by bacterial lipopolysaccharide (LPS): multifocal effects of LPS-induced suppression of the primary antibody response to a T-dependent antigen.细菌脂多糖(LPS)对免疫反应的调节:LPS诱导对T细胞依赖性抗原的初次抗体反应抑制的多焦点效应
J Immunol. 1978 Dec;121(6):2340-6.
10
Immunologic suppression after oral administration of antigen. I. Specific suppressor cells formed in rat Peyer's patches after oral administration of sheep erythrocytes and their systemic migration.口服抗原后的免疫抑制。I. 口服绵羊红细胞后大鼠派伊尔结中形成的特异性抑制细胞及其全身迁移。
J Immunol. 1978 Nov;121(5):1878-83.

C3H/HeJ小鼠中缺乏口服耐受。

Lack of oral tolerance in C3H/HeJ mice.

作者信息

Kiyono H, McGhee J R, Wannemuehler M J, Michalek S M

出版信息

J Exp Med. 1982 Feb 1;155(2):605-10. doi: 10.1084/jem.155.2.605.

DOI:10.1084/jem.155.2.605
PMID:7035600
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC2186596/
Abstract

Daily gastric intubation of lipopolysaccharide (LPS)-responsive C3H/HeN, BALB/c, and Swiss mice with SRBC for 2 wk resulted in oral tolerance, whereas similarly treated LPS-nonresponsive C3H/HeJ mice gave splenic anti-SRBC PFC responses, including the IgA isotype, after systemic challenge with antigen. Oral tolerance in LPS-responsive C3H/HeN mice was due to T suppressor (Ts) cells because significant Ts cell activity was demonstrated in both Peyer's patches (PP) and spleens of these animals. On the other hand, T cells from PP and spleens of identically treated C3H/HeJ mice exhibited mainly T helper cell activity. Prior treatment of PP or spleen cell preparations from tolerant C3H/HeN mice with anti-Lyt-2.1 resulted in good in vitro anti-SRBC PFC responses, especially IgA isotype responses in PP cell cultures. These results indicate that oral administration of a thymic-dependent antigen (SRBC) to LPS-responsive mice induced a Ts cell population in PP, which, after migration to peripheral lymphoid tissue (e.g., spleen), suppressed responses to systemically administered antigen. LPS-nonresponsive mice lack this Ts cell pathway and continually respond to oral administration of antigen.

摘要

每天给对脂多糖(LPS)有反应的C3H/HeN、BALB/c和瑞士小鼠经胃插管注入绵羊红细胞(SRBC),持续2周,可诱导口服耐受,而同样处理的对LPS无反应的C3H/HeJ小鼠在经抗原全身攻击后,脾脏产生抗SRBC的空斑形成细胞(PFC)反应,包括IgA同种型反应。LPS反应性C3H/HeN小鼠的口服耐受是由于T抑制细胞(Ts),因为在这些动物的派尔集合淋巴结(PP)和脾脏中均显示出显著的Ts细胞活性。另一方面,经同样处理的C3H/HeJ小鼠的PP和脾脏中的T细胞主要表现出T辅助细胞活性。用抗Lyt-2.1预先处理来自耐受C3H/HeN小鼠的PP或脾细胞制剂,可在体外产生良好的抗SRBC PFC反应,尤其是PP细胞培养物中的IgA同种型反应。这些结果表明,给LPS反应性小鼠口服胸腺依赖性抗原(SRBC)可在PP中诱导产生Ts细胞群,该细胞群迁移至外周淋巴组织(如脾脏)后,可抑制对全身给予抗原的反应。LPS无反应性小鼠缺乏这种Ts细胞途径,并且持续对口服抗原产生反应。