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1
An investigation of the nature of induced suppression to experimental autoimmune thyroiditis.对实验性自身免疫性甲状腺炎诱导抑制性质的研究。
Immunology. 1988 Feb;63(2):199-203.
2
Suppression in experimental autoimmune thyroiditis: the role of unique and shared determinants on mouse thyroglobulin in self-tolerance.实验性自身免疫性甲状腺炎中的抑制作用:小鼠甲状腺球蛋白上独特和共享决定簇在自身耐受中的作用。
Cell Immunol. 1990 Nov;131(1):140-9. doi: 10.1016/0008-8749(90)90241-i.
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Characterization of resistance to murine experimental autoimmune thyroiditis: duration and afferent action of thyroglobulin- and TSH-induced suppression.对小鼠实验性自身免疫性甲状腺炎抗性的特征:甲状腺球蛋白和促甲状腺激素诱导抑制的持续时间及传入作用
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Intravenous administration of deaggregated mouse thyroglobulin suppresses induction of experimental autoimmune thyroiditis and expression of both Th1 and Th2 cytokines.静脉注射去聚合的小鼠甲状腺球蛋白可抑制实验性自身免疫性甲状腺炎的诱导以及Th1和Th2细胞因子的表达。
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Synergism between mouse thyroglobulin- and vaccination-induced suppressor mechanisms in murine experimental autoimmune thyroiditis.小鼠甲状腺球蛋白与疫苗接种诱导的抑制机制在小鼠实验性自身免疫性甲状腺炎中的协同作用。
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Activation of cytotoxic T cells and effector cells in experimental autoimmune thyroiditis by shared determinants of mouse and human thyroglobulins.小鼠和人甲状腺球蛋白的共同决定簇激活实验性自身免疫性甲状腺炎中的细胞毒性T细胞和效应细胞。
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Differential requirement for autoantibody-producing B cells for induction of lymphocytic versus granulomatous experimental autoimmune thyroiditis.产生自身抗体的B细胞在诱导淋巴细胞性与肉芽肿性实验性自身免疫性甲状腺炎中的差异需求。
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CD40L is necessary for the priming of effector cells for lymphocytic and granulomatous experimental autoimmune thyroiditis.CD40L对于淋巴细胞性和肉芽肿性实验性自身免疫性甲状腺炎效应细胞的启动是必需的。
J Autoimmun. 1999 Feb;12(1):1-12. doi: 10.1006/jaut.1998.0256.
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Distinctive modulation by IL-4 and IL-10 of the effector function of murine thyroglobulin-primed cells in "transfer-experimental autoimmune thyroiditis".白细胞介素-4和白细胞介素-10对“转移实验性自身免疫性甲状腺炎”中鼠甲状腺球蛋白致敏细胞效应功能的独特调节作用
Cell Immunol. 1995 May;162(2):171-7. doi: 10.1006/cimm.1995.1066.

引用本文的文献

1
Abnormalities in the SJL mouse provide evidence for different mechanisms for the induction and transfer of tolerance to mouse thyroglobulin.SJL小鼠的异常情况为诱导和传递对小鼠甲状腺球蛋白的耐受性的不同机制提供了证据。
Immunology. 1989 Jan;66(1):106-10.
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Anti-CD44 treatment does not prevent the extravasation of autopathogenic T cells to the thyroid in experimental autoimmune thyroiditis.在实验性自身免疫性甲状腺炎中,抗CD44治疗并不能阻止自身致病性T细胞向甲状腺的外渗。
Immunology. 1999 Jul;97(3):533-9. doi: 10.1046/j.1365-2567.1999.00783.x.
3
Identification of a thyroxine-containing self-epitope of thyroglobulin which triggers thyroid autoreactive T cells.鉴定甲状腺球蛋白中含甲状腺素的自身表位,该表位可触发甲状腺自身反应性T细胞。
J Exp Med. 1991 Aug 1;174(2):363-70. doi: 10.1084/jem.174.2.363.

本文引用的文献

1
IMMUNOLOGICAL UNRESPONSIVENESS TO PROTEIN ANTIGENS IN RABBITS. I. THE DURATION OF UNRESPONSIVENESS FOLLOWING A SINGLE INJECTION AT BIRTH.兔子对蛋白质抗原的免疫无反应性。I. 出生时单次注射后无反应性的持续时间。
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2
Tolerance to thyroglobulin by activating suppressor mechanisms.
Ann N Y Acad Sci. 1982;392:191-209. doi: 10.1111/j.1749-6632.1982.tb36108.x.
3
The termination of immunological unresponsiveness to bovine serum albumin in rabbits. I. Quantitative and qualitative response to cross-reacting albumins.兔对牛血清白蛋白免疫无反应性的终止。I. 对交叉反应白蛋白的定量和定性反应。
J Exp Med. 1970 Jul 1;132(1):66-76. doi: 10.1084/jem.132.1.66.
4
Murine thyroiditis: importance of adjuvant and mouse strain for the induction of thyroid lesions.小鼠甲状腺炎:佐剂和小鼠品系在诱导甲状腺病变中的重要性。
J Immunol. 1971 Mar;106(3):698-704.
5
Recent observations and concepts in immunological unresponsiveness and autoimmunity.免疫无反应性与自身免疫性的近期观察结果及相关概念
Clin Exp Immunol. 1971 Oct;9(4):437-47.
6
Antigenic determinants of human thyroglobulin differentiated using antigen fragments.利用抗原片段鉴定的人甲状腺球蛋白的抗原决定簇。
Immunology. 1985 Mar;54(3):419-27.
7
Recognition of thyroglobulin autoantigenic epitopes by murine T and B cells.小鼠T细胞和B细胞对甲状腺球蛋白自身抗原表位的识别。
Immunology. 1987 Oct;62(2):255-63.

对实验性自身免疫性甲状腺炎诱导抑制性质的研究。

An investigation of the nature of induced suppression to experimental autoimmune thyroiditis.

作者信息

Parish N M, Rayner D, Cooke A, Roitt I M

机构信息

Department of Immunology, Middlesex Hospital Medical School, London, U.K.

出版信息

Immunology. 1988 Feb;63(2):199-203.

PMID:2450834
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC1454523/
Abstract

When mice are pretreated with soluble mouse thyroglobulin (MTg), subsequent induction of autoantibodies in experimental allergic thyroiditis (EAT) is suppressed. This suppression can be reproducibly transferred to low-level irradiated syngeneic recipients and is specific for MTg. Injection of normal cells does not reverse this tolerance, also indicative of an active suppression. Neither can the induced unresponsiveness be overcome by immunization with cross-reactive xenogeneic Tg; although antibodies are formed which will bind to MTg, these are not to epitopes to which antibodies are normally formed on immunization or towards which tolerance is induced. This implies that tolerance might be induced at least at the B-cell level, a view supported by the inability of DNP to provide a new carrier to break tolerance when conjugated to MTg. The poorer response to DNP in these animals also suggests anergy of the MTg-specific T helpers.

摘要

当用可溶性小鼠甲状腺球蛋白(MTg)对小鼠进行预处理时,实验性过敏性甲状腺炎(EAT)中自身抗体的后续诱导会受到抑制。这种抑制作用可重复转移至低剂量照射的同基因受体,且对MTg具有特异性。注射正常细胞并不能逆转这种耐受性,这也表明存在主动抑制。用交叉反应性异种甲状腺球蛋白(Tg)免疫也无法克服诱导的无反应性;尽管会形成能与MTg结合的抗体,但这些抗体针对的不是免疫时通常形成抗体的表位,也不是诱导耐受性时针对的表位。这意味着耐受性可能至少在B细胞水平被诱导,当DNP与MTg偶联时无法提供新的载体来打破耐受性,这一观点得到了支持。这些动物对DNP的反应较差也表明MTg特异性T辅助细胞存在无反应性。