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Antigen-specific tolerance induction and the immunotherapy of experimental autoimmune disease.抗原特异性耐受诱导与实验性自身免疫病的免疫治疗
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2
T cell response of I-Aq mice to self type II collagen: meshing of the binding motif of the I-Aq molecule with repetitive sequences results in autoreactivity to multiple epitopes.I-Aq小鼠对自身II型胶原蛋白的T细胞反应:I-Aq分子的结合基序与重复序列相匹配导致对多个表位的自身反应性。
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The importance of the back-signal from T cells into antigen-presenting cells in determining susceptibility to parasites.T细胞向抗原呈递细胞发出的反向信号在决定对寄生虫易感性方面的重要性。
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Thalidomide therapy of established collagen-induced arthritis (CIA) not accompanied by an evident Th2 shift.沙利度胺治疗已确诊的胶原诱导性关节炎(CIA),且未伴有明显的Th2偏移。
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Suppression of murine collagen-induced arthritis by nasal administration of collagen.通过鼻腔给予胶原蛋白抑制小鼠胶原诱导性关节炎
Immunology. 1997 Feb;90(2):161-4. doi: 10.1046/j.1365-2567.1997.00191.x.
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Type II collagen serology: a guide to clinical responsiveness to oral tolerance?II型胶原血清学:口腔耐受临床反应性的指南?
Rheumatol Int. 1997;16(6):237-40. doi: 10.1007/BF01375655.
7
Peptide-induced nasal tolerance for a mycobacterial heat shock protein 60 T cell epitope in rats suppresses both adjuvant arthritis and nonmicrobially induced experimental arthritis.肽诱导大鼠对分枝杆菌热休克蛋白60 T细胞表位产生鼻耐受,可抑制佐剂性关节炎和非微生物诱导的实验性关节炎。
Proc Natl Acad Sci U S A. 1997 Apr 1;94(7):3284-9. doi: 10.1073/pnas.94.7.3284.
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Oral tolerance for the treatment of autoimmune diseases.口服耐受用于自身免疫性疾病的治疗。
Annu Rev Med. 1997;48:341-51. doi: 10.1146/annurev.med.48.1.341.
9
Antigen organization regulates cluster formation and induction of cytotoxic T lymphocytes by helper T cell subsets.抗原组织通过辅助性T细胞亚群调节细胞毒性T淋巴细胞的簇形成和诱导。
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Protective major histocompatibility complex genes and the role of interleukin-4 in collagen-induced arthritis.主要组织相容性复合体保护性基因及白细胞介素-4在胶原诱导性关节炎中的作用。
Eur J Immunol. 1996 Dec;26(12):3234-7. doi: 10.1002/eji.1830261259.

通过长期鼻腔给予自身II型胶原肽对小鼠胶原诱导性关节炎的旁观者抑制作用

Bystander suppression of murine collagen-induced arthritis by long-term nasal administration of a self type II collagen peptide.

作者信息

Bayrak S, Mitchison N A

机构信息

Deutsches Rheumaforschungszentrum, Berlin, Germany.

出版信息

Clin Exp Immunol. 1998 Jul;113(1):92-5. doi: 10.1046/j.1365-2249.1998.00638.x.

DOI:10.1046/j.1365-2249.1998.00638.x
PMID:9697989
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC1905015/
Abstract

Oral and more recently nasal tolerance have attracted attention as potential treatments of autoimmune disease. Arthritis induced by bovine type II collagen (CII) is a widely used animal model of rheumatoid arthritis, which is here used to investigate the efficacy of nasal treatment by a short peptide. The peptide spans residues 707-721 (designated p707), an epitope of mouse CII that is most strongly recognized after immunization of mice with this self-protein. The treatment was partially effective, but almost only when the peptide was administered in large doses over a prolonged period. Mice immunized with bovine CII respond mainly to other peptides, located in the CB11 fragment around amino acid residues 256-270. The tolerance effect therefore results from intramolecular suppression, between epitopes located in different parts of this large protein.

摘要

口服耐受性以及最近的鼻内耐受性作为自身免疫性疾病的潜在治疗方法已引起关注。牛II型胶原蛋白(CII)诱导的关节炎是类风湿性关节炎广泛使用的动物模型,在此用于研究短肽鼻内治疗的疗效。该肽跨越第707 - 721位氨基酸残基(命名为p707),是小鼠CII的一个表位,在用这种自身蛋白免疫小鼠后,该表位得到最强烈的识别。该治疗部分有效,但几乎仅在长时间大剂量给予该肽时才有效。用牛CII免疫的小鼠主要对位于氨基酸残基256 - 270周围的CB11片段中的其他肽产生反应。因此,耐受效应是由位于这种大蛋白不同部位的表位之间的分子内抑制引起的。