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1
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.
2
Isotype-specific immunoregulation. Systemic antigen induces splenic T contrasuppressor cells which support IgM and IgG subclass but not IgA responses.同型特异性免疫调节。全身性抗原诱导脾T抗抑制细胞,该细胞支持IgM和IgG亚类反应,但不支持IgA反应。
J Immunol. 1988 Mar 1;140(5):1385-92.
3
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。
J Immunol. 1983 Dec;131(6):2616-22.
4
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。
J Immunol. 1987 Nov 15;139(10):3251-9.
5
Role of the galt contrasuppressor T cell circuit in isotype-specific immunoregulation.肠道相关淋巴组织反抑制性T细胞回路在同种型特异性免疫调节中的作用。
Adv Exp Med Biol. 1988;237:649-53. doi: 10.1007/978-1-4684-5535-9_98.
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。
Microbiol Immunol. 1984;28(3):261-80. doi: 10.1111/j.1348-0421.1984.tb00679.x.
7
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。
J Immunol. 1984 Apr;132(4):1702-11.
8
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.
9
Isotype specificity of helper T cell clones. Peyer's patch Th cells preferentially collaborate with mature IgA B cells for IgA responses.辅助性T细胞克隆的同种型特异性。派尔集合淋巴结的Th细胞优先与成熟的IgA B细胞协作以产生IgA应答。
J Exp Med. 1984 Mar 1;159(3):798-811. doi: 10.1084/jem.159.3.798.
10
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。
J Immunol. 1986 Jun 15;136(12):4414-9.

引用本文的文献

1
Vaccination strategies for mucosal immune responses.黏膜免疫反应的疫苗接种策略。
Clin Microbiol Rev. 2001 Apr;14(2):430-45. doi: 10.1128/CMR.14.2.430-445.2001.
2
Induction of apoptosis in WEHI 231 cells by cationic liposomes.阳离子脂质体诱导WEHI 231细胞凋亡
Pharm Res. 2000 May;17(5):515-20. doi: 10.1023/a:1007552529280.
3
alpha 2-macroglobulin stimulation of protein tyrosine phosphorylation in macrophages via the mannose receptor for Fc gamma receptor-mediated phagocytosis activation.α2-巨球蛋白通过甘露糖受体刺激巨噬细胞中的蛋白质酪氨酸磷酸化,用于Fcγ受体介导的吞噬作用激活。
Immunology. 1996 Nov;89(3):436-41. doi: 10.1046/j.1365-2567.1996.d01-765.x.
4
The contribution of a serum component(s) modified by B cells to the mechanism for macrophage activation by liposomes.经B细胞修饰的血清成分对脂质体激活巨噬细胞机制的贡献。
Immunology. 1993 Oct;80(2):253-8.
5
A review of the mechanisms of oral tolerance and immunotherapy.口服耐受与免疫治疗机制综述。
J R Soc Med. 1995 Jan;88(1):14-7.
6
Identification of the serum factor required for liposome-primed activation of mouse peritoneal macrophages. Modified alpha 2-macroglobulin enhances Fc gamma receptor-mediated phagocytosis of opsonized sheep red blood cells.鉴定脂质体引发的小鼠腹腔巨噬细胞激活所需的血清因子。修饰的α2-巨球蛋白增强Fcγ受体介导的调理绵羊红细胞的吞噬作用。
Immunology. 1995 Sep;86(1):64-70.
7
Modification of alpha 2-macroglobulin into a macrophage-activating factor through the action of liposome-stimulated B-cell membranous glycosidases.通过脂质体刺激的B细胞膜糖苷酶的作用将α2-巨球蛋白修饰为巨噬细胞激活因子。
Immunology. 1995 Sep;86(1):58-63.
8
Enteric immunization reveals a T cell network for IgA responses and suggests that humans possess a common mucosal immune system.肠道免疫揭示了一个针对IgA应答的T细胞网络,并表明人类拥有共同的黏膜免疫系统。
Antonie Van Leeuwenhoek. 1987;53(6):537-43. doi: 10.1007/BF00415514.
9
Combined parenteral and oral immunization results in an enhanced mucosal immunoglobulin A response to Shigella flexneri.肠胃外与口服联合免疫可增强对福氏志贺菌的黏膜免疫球蛋白A反应。
Infect Immun. 1988 Apr;56(4):910-5. doi: 10.1128/iai.56.4.910-915.1988.
10
A novel mechanism for the selection of isotype-specific antibody responses: the role of intestinal T cells in the regulation of IgA synthesis by the anti-suppressor circuit.一种选择同种型特异性抗体应答的新机制:肠道T细胞在抗抑制回路调节IgA合成中的作用。
Immunology. 1988 Sep;65(1):59-66.

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
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.
3
Mucosal immunology.黏膜免疫学
Immunology. 1980 Oct;41(2):249-70.
4
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。
Proc Natl Acad Sci U S A. 1982 Jan;79(2):596-600. doi: 10.1073/pnas.79.2.596.
5
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.
6
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.
7
Microenvironmental immunoregulation: possible role of contrasuppressor cells in maintaining immune responses in gut-associated lymphoid tissues.微环境免疫调节:抗抑制细胞在维持肠道相关淋巴组织免疫反应中的可能作用。
Proc Natl Acad Sci U S A. 1982 Feb;79(3):889-92. doi: 10.1073/pnas.79.3.889.
8
Lipopolysaccharide (LPS) regulation of the immune response: LPS influence on oral tolerance induction.脂多糖(LPS)对免疫反应的调节:LPS对口服耐受诱导的影响。
J Immunol. 1982 May;128(5):1992-8.
9
Immunoregulatory circuits which modulate responsiveness to suppressor cell signals: contrasuppressor cells can convert an in vivo tolerogenic signal into an immunogenic one.调节对抑制细胞信号反应性的免疫调节回路:抗抑制细胞可将体内致耐受性信号转化为免疫原性信号。
Eur J Immunol. 1981 Dec;11(12):980-3. doi: 10.1002/eji.1830111206.
10
Immunoregulatory circuits which modulate responsiveness to suppressor cell signals: characterization of an effector cell in the contrasuppressor circuit.调节对抑制细胞信号反应性的免疫调节环路:反抑制环路中效应细胞的特性
Eur J Immunol. 1981 Dec;11(12):973-80. doi: 10.1002/eji.1830111205.

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。

Isotype-specific immunoregulation. Evidence for a distinct subset of T contrasuppressor cells for IgA responses in murine Peyer's patches.

作者信息

Suzuki I, Kitamura K, Kiyono H, Kurita T, Green D R, McGhee J R

出版信息

J Exp Med. 1986 Aug 1;164(2):501-16. doi: 10.1084/jem.164.2.501.

DOI:10.1084/jem.164.2.501
PMID:2941516
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC2188238/
Abstract

The ability of murine Peyer's patch (PP) T contrasuppressor cells (Tcs) to reverse oral tolerance to the T cell-dependent (TD) antigen SRBC was studied both in vivo and in vitro. C3H/HeJ mice given SRBC orally for 4 wk are not rendered tolerant to this antigen and were used as a source of PP Tcs cells for adoptive transfer to identically treated, orally tolerized C3H/HeN mice. Transfer of 10(4) or 5 X 10(4) V. villosa-adherent PP T cells resulted in splenic IgM, IgG, and mainly IgA responses in C3H/HeN mice challenged systemically with SRBC. The T cell responsible was Lyt-1+, 2-, L3T4-, I-JK+ and V. villosa lectin-adherent, all characteristics of mature effector Tcs cells. This C3H/HeJ PP Tcs cell subset was also effective when added to in vitro cultures of tolerized spleen cells derived from SRBC-fed, C3H/HeN mice. Interestingly, C3H/HeJ PP Tcs cells restored mainly IgA responses when transferred in vivo or when added to suppressed C3H/HeN splenic cultures. Comparison of the functional activity of Tcs cells derived from spleen or PP of orally immunized C3H/HeJ mice revealed that splenic Tcs cells supported responses of all 3 isotypes; however, PP Tcs cells yielded three-fourfold higher IgA responses, when compared with IgM or IgG anti-SRBC responses. Adherence of C3H/HeJ PP Tcs to an Fc alpha R+ T cell line derived from IgA-specific Th cells resulted in a nonadherent cell fraction that potentiated only IgM and IgG responses, while bound Tcs cells preferentially supported IgA responses. These results suggest that murine PP contain IgA-specific Tcs cells that allow IgA response induction in the presence of Ts cells that mediate oral tolerance.

摘要

对小鼠派伊尔结(PP)T 辅助抑制细胞(Tcs)逆转对 T 细胞依赖性(TD)抗原绵羊红细胞(SRBC)口服耐受的能力进行了体内和体外研究。口服 SRBC 4 周的 C3H/HeJ 小鼠对该抗原未产生耐受,这些小鼠被用作 PP Tcs 细胞的来源,用于过继转移到经相同处理且口服耐受的 C3H/HeN 小鼠体内。转移 10⁴ 或 5×10⁴ 个绒毛状黏附的 PP T 细胞,可使经 SRBC 全身攻击的 C3H/HeN 小鼠产生脾脏 IgM、IgG,主要是 IgA 应答。起作用的 T 细胞为 Lyt-1⁺、2⁻、L3T4⁻、I-JK⁺ 且为绒毛状凝集素黏附型,这些都是成熟效应 Tcs 细胞的特征。当将该 C3H/HeJ PP Tcs 细胞亚群添加到来自喂食 SRBC 的 C3H/HeN 小鼠的耐受脾细胞的体外培养物中时,也具有效果。有趣的是,C3H/HeJ PP Tcs 细胞在体内转移或添加到受抑制 的C3H/HeN 脾脏培养物中时,主要恢复 IgA 应答。对口服免疫的 C3H/HeJ 小鼠脾脏或 PP 来源的 Tcs 细胞的功能活性进行比较发现,脾脏 Tcs 细胞支持所有三种同种型的应答;然而,与 IgM 或 IgG 抗 SRBC 应答相比,PP Tcs 细胞产生的 IgA 应答高出三倍。C3H/HeJ PP Tcs 与源自 IgA 特异性 Th 细胞的 FcαR⁺ T 细胞系黏附后,产生的非黏附细胞部分仅增强 IgM 和 IgG 应答,而结合的 Tcs 细胞则优先支持 IgA 应答。这些结果表明,小鼠 PP 中含有 IgA 特异性 Tcs 细胞,在介导口服耐受的 Ts 细胞存在的情况下,这些细胞可诱导 IgA 应答。