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1
Passive transfer of unresponsiveness by lymph node cells. Studies on adjuvant disease.淋巴结细胞介导的无反应性被动转移。佐剂病研究。
Immunology. 1975 Apr;28(4):703-10.
2
Studies on the mechanism of specific immunological unresponsiveness. II. Immunological properties of lymphoid cells from normal, immunized and immunologically unresponsive mice transferred into lethally irradiated recipients.特异性免疫无反应性机制的研究。II. 来自正常、免疫和免疫无反应小鼠的淋巴细胞转移至致死性照射受体后的免疫特性。
Z Immunitatsforsch Exp Klin Immunol. 1976 Mar;151(1-2):22-31.
3
Studies on the mechanism of unresponsiveness. Inability of lymph node cells from pretreated donor rats to transfer adjuvant disease.无反应机制的研究。预处理供体大鼠的淋巴结细胞无法传递佐剂病。
Medicina (B Aires). 1975 Mar-Apr;35(2):133-40.
4
Suppression of collagen type II-induced arthritis by transfer of lymphoid cells from rats immunized with collagen.通过转移用胶原蛋白免疫的大鼠的淋巴细胞来抑制II型胶原诱导的关节炎。
Clin Exp Immunol. 1985 Aug;61(2):368-72.
5
Adjuvant oil induces waves of arthritogenic lymph node cells prior to arthritis onset.佐剂油在关节炎发作前诱导致关节炎淋巴结细胞波动。
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6
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7
Inhibition of adjuvant-induced arthritis by interleukin-10-driven regulatory cells induced via nasal administration of a peptide analog of an arthritis-related heat-shock protein 60 T cell epitope.通过经鼻给予关节炎相关热休克蛋白60 T细胞表位的肽类似物诱导的白细胞介素-10驱动的调节性细胞对佐剂诱导的关节炎的抑制作用。
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8
Oil-induced arthritis in DA rats passive transfer by T cells but not with serum.油诱导的关节炎在DA大鼠中可通过T细胞进行被动转移,但血清不能。
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9
Studies on the role of suppressor cells in specific unresponsiveness to DNCB.关于抑制细胞在对二硝基氯苯特异性无反应性中的作用的研究。
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10
Experimental Salmonella typhimurium infections in rats. II. Active and passive immunization as protection against a lethal bacterial dose.
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引用本文的文献

1
Autoimmunity to collagen in adjuvant arthritis of rats.大鼠佐剂性关节炎中对胶原蛋白的自身免疫反应。
J Clin Invest. 1980 Nov;66(5):1109-17. doi: 10.1172/JCI109940.
2
Epithelioid granuloma induced by muramyl dipeptide in immunologically deficient rats.免疫缺陷大鼠中胞壁酰二肽诱导的上皮样肉芽肿
Infect Immun. 1981 Dec;34(3):993-9. doi: 10.1128/iai.34.3.993-999.1981.
3
Characterization of low dose induced suppressor cells in adjuvant arthritis in rats.大鼠佐剂性关节炎中低剂量诱导抑制细胞的特性研究
Clin Exp Immunol. 1983 Jul;53(1):60-6.
4
In vivo treatment with W3/13 (anti-pan T) but not with OX8 (anti-suppressor/cytotoxic T) monoclonal antibodies impedes the development of adjuvant arthritis in rats.用W3/13(抗全T细胞)单克隆抗体而非OX8(抗抑制/细胞毒性T细胞)单克隆抗体进行体内治疗,可阻碍大鼠佐剂性关节炎的发展。
Immunology. 1985 Nov;56(3):383-91.
5
Effect of testosterone on the kinetics of the development of suppressor cells in adjuvant arthritis.睾酮对佐剂性关节炎中抑制细胞发育动力学的影响。
Experientia. 1985 Oct 15;41(10):1337-8. doi: 10.1007/BF01952083.
6
The 65-kDa heat-shock protein in the pathogenesis, prevention and therapy of autoimmune arthritis and diabetes mellitus in rats and mice.65千道尔顿热休克蛋白在大鼠和小鼠自身免疫性关节炎及糖尿病发病机制、预防和治疗中的作用
Springer Semin Immunopathol. 1991;13(1):99-113. doi: 10.1007/BF01225281.

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INDUCTION OF IMMUNOLOGICAL PARALYSIS IN TWO ZONES OF DOSAGE.两个剂量区免疫麻痹的诱导
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2
PASSIVE TRANSFER OF ADJUVANT ARTHRITIS BY LYMPH NODE OR SPLEEN CELLS.佐剂性关节炎通过淋巴结或脾细胞的被动转移
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FURTHER IMMUNOLOGIC STUDIES OF ADJUVANT DISEASE IN THE RAT.大鼠佐剂病的进一步免疫学研究。
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PASSIVE TRANSFER OF ADJUVANT ARTHRITIS IN RATS WITH LIVING LYMPHOID CELLS OF SENSITIZED DONORS.用致敏供体的活淋巴细胞将佐剂性关节炎被动转移至大鼠体内。
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Protection of rats against adjuvant arthritis by bacterial lipoplysaccharides.细菌脂多糖对大鼠佐剂性关节炎的保护作用。
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6
Studies of arthritis and other lesions induced in rats by injection of mycobacterial adjuvant. II. Evidence that the disease is a disseminated immunologic response to exogenous antigen.关于注射分枝杆菌佐剂诱导大鼠产生关节炎及其他病变的研究。II. 该疾病是对外源抗原的一种播散性免疫反应的证据。
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Arthritogenicity and protective effect against adjuvant arthritis of wax Ds fractions (glycolipids without a nitrogen-containing moiety) of Mycobacterium tuberculosis var. hominis and bovis.人型和牛型结核分枝杆菌蜡质D组分(不含含氮部分的糖脂)的致关节炎性及对佐剂性关节炎的保护作用
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8
Studies of the mechanism whereby adjuvant disease is suppressed in rats pretreated with mycobacteria.对用分枝杆菌预处理的大鼠中佐剂病被抑制的机制的研究。
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Tolerance in adult rabbits by repeated non-immunogenic doses of bovine serum albumin.通过重复给予非免疫原性剂量的牛血清白蛋白诱导成年兔产生耐受性。
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淋巴结细胞介导的无反应性被动转移。佐剂病研究。

Passive transfer of unresponsiveness by lymph node cells. Studies on adjuvant disease.

作者信息

Eugui E M, Houssay R H

出版信息

Immunology. 1975 Apr;28(4):703-10.

PMID:1097332
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC1445832/
Abstract

Pretreatment of rats with subarthritogenic doses of mycobacterial adjuvant suppresses the arthritogenic reaction induced by this adjuvant. This unresponsiveness can betransferred to normal syngeneic recipients by viable lymph node cells from unresponsivedonors. Serum from the same donors did not prevent the arthritis. Abrogation ofunresponsiveness was obtained by injecting normal lymph node cells together with the challeging inoculation and also with sensitized lymphoid cells. In agreement with the concept of tolerance as an active immune reaction, the data suggest that in this experimental model lymphoid cells actively suppress the immune response induced by microbacterial adjuvant. Thus, arthritis or unresponsiveness may result from the predominance of either sensitized or suppressor cells.

摘要

用亚致关节炎剂量的分枝杆菌佐剂对大鼠进行预处理,可抑制该佐剂诱导的致关节炎反应。这种无反应性可通过来自无反应供体的活淋巴结细胞转移给正常的同基因受体。来自相同供体的血清不能预防关节炎。通过将正常淋巴结细胞与激发接种物以及致敏淋巴细胞一起注射,可消除无反应性。与耐受性作为一种主动免疫反应的概念一致,数据表明在该实验模型中,淋巴细胞可积极抑制由微生物佐剂诱导的免疫反应。因此,关节炎或无反应性可能是由于致敏细胞或抑制细胞占优势所致。