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本文引用的文献

1
Protective role of NK1.1+ cells in experimental Staphylococcus aureus arthritis.NK1.1⁺细胞在实验性金黄色葡萄球菌关节炎中的保护作用。
Clin Exp Immunol. 1999 Jul;117(1):63-9. doi: 10.1046/j.1365-2249.1999.00922.x.
2
Susceptibility to oil-induced arthritis is linked to Oia2 on chromosome 4 in a DA(DA x PVG.1AV1) backcross.在DA(DA×PVG.1AV1)回交群体中,对油诱导性关节炎的易感性与4号染色体上的Oia2相关。
Transplant Proc. 1999 May;31(3):1597-9. doi: 10.1016/s0041-1345(99)00052-4.
3
Identification of arthritogenic adjuvants of self and foreign origin.鉴定自身来源和外来来源的致关节炎佐剂。
Scand J Immunol. 1999 Jan;49(1):45-50. doi: 10.1046/j.1365-3083.1999.00463.x.
4
Signalling through NK1.1 triggers NK cells to die but induces NK T cells to produce interleukin-4.通过NK1.1发出的信号会触发自然杀伤细胞死亡,但会诱导自然杀伤T细胞产生白细胞介素-4。
Immunology. 1998 Feb;93(2):296-305. doi: 10.1046/j.1365-2567.1998.00422.x.
5
Role of natural killer cells and TCR gamma delta T cells in acute autoimmune encephalomyelitis.自然杀伤细胞和TCRγδ T细胞在急性自身免疫性脑脊髓炎中的作用。
Eur J Immunol. 1998 May;28(5):1681-8. doi: 10.1002/(SICI)1521-4141(199805)28:05<1681::AID-IMMU1681>3.0.CO;2-T.
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Identification of rat susceptibility loci for adjuvant-oil-induced arthritis.鉴定佐剂油诱导性关节炎大鼠的易感性基因座。
Proc Natl Acad Sci U S A. 1998 May 26;95(11):6383-7. doi: 10.1073/pnas.95.11.6383.
7
alpha/beta-T cell receptor (TCR)+CD4-CD8- (NKT) thymocytes prevent insulin-dependent diabetes mellitus in nonobese diabetic (NOD)/Lt mice by the influence of interleukin (IL)-4 and/or IL-10.α/β-T细胞受体(TCR)+CD4-CD8-(自然杀伤T细胞,NKT)胸腺细胞通过白细胞介素(IL)-4和/或IL-10的作用预防非肥胖糖尿病(NOD)/Lt小鼠的胰岛素依赖型糖尿病。
J Exp Med. 1998 Apr 6;187(7):1047-56. doi: 10.1084/jem.187.7.1047.
8
Regulation of experimental autoimmune encephalomyelitis by natural killer (NK) cells.自然杀伤(NK)细胞对实验性自身免疫性脑脊髓炎的调节作用。
J Exp Med. 1997 Nov 17;186(10):1677-87. doi: 10.1084/jem.186.10.1677.
9
Polyclonal Th1 cells transfer oil-induced arthritis.多克隆Th1细胞可转移油诱导的关节炎。
Immunology. 1997 Jun;91(2):260-5. doi: 10.1046/j.1365-2567.1997.00251.x.
10
Negative regulation of rat natural killer cell activity by major histocompatibility complex class I recognition.主要组织相容性复合体I类识别对大鼠自然杀伤细胞活性的负调控
Eur J Immunol. 1996 Nov;26(11):2582-6. doi: 10.1002/eji.1830261107.

CD8 + 细胞可抑制油诱导的关节炎。

CD8+ cells suppress oil-induced arthritis.

作者信息

Jansson A M, Lorentzen J C, Bucht A

机构信息

Department of Medicine, Unit of Rheumatology, Karolinska Institute, Stockholm, Sweden.

出版信息

Clin Exp Immunol. 2000 Jun;120(3):532-6. doi: 10.1046/j.1365-2249.2000.01241.x.

DOI:10.1046/j.1365-2249.2000.01241.x
PMID:10844534
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC1905569/
Abstract

Oil-induced arthritis is a genetically restricted polyarthritis that develops in the DA rat after injection of the mineral oil Freund's incomplete adjuvant. Here, we investigated the role of the potentially disease-limiting cell populations CD8+ T cells, gammadelta T cells, natural killer (NK) cells and NK T cells in inguinal lymph nodes for the development of this adjuvant-induced arthritis. Flow cytometry analysis before and at disease onset revealed a higher proportion of lymph node T cells expressing NKR-P1 in the disease-resistant LEW.1AV1 compared with the disease-susceptible DA strain, suggesting that NK T cells might be disease protective. However, prophylactic in vivo administration of an anti-NKR-P1 MoAb (clone 10/78) did not consistently affect the disease course. The proportion of CD8+ T cells and the ratio CD4+/CD8+ T cells in inguinal lymph nodes did not differ significantly between DA and LEW.1AV1 rats before or at disease onset. Nevertheless, prophylactic in vivo depletion of CD8+ cells by the OX8 MoAb in the DA strain resulted in an earlier disease onset compared with the control group, demonstrating that CD8+ cells regulate arthritis development. In vivo depletion of gammadelta T cells by the V65 MoAb did not alter the disease course, indicating that the disease-suppressive CD8+ cells are alphabeta T cells or NK cells.

摘要

油诱导性关节炎是一种基因受限的多关节炎,在给DA大鼠注射矿物油弗氏不完全佐剂后发生。在此,我们研究了腹股沟淋巴结中潜在的疾病限制细胞群体CD8 + T细胞、γδ T细胞、自然杀伤(NK)细胞和NK T细胞在这种佐剂诱导性关节炎发展中的作用。疾病发作前和发作时的流式细胞术分析显示,与疾病易感的DA品系相比,抗病的LEW.1AV1品系中表达NKR-P1的淋巴结T细胞比例更高,这表明NK T细胞可能具有疾病保护作用。然而,预防性体内给予抗NKR-P1单克隆抗体(克隆10/78)并未始终影响疾病进程。在疾病发作前或发作时,DA和LEW.1AV1大鼠腹股沟淋巴结中CD8 + T细胞的比例以及CD4 + /CD8 + T细胞的比例没有显著差异。尽管如此,DA品系中通过OX8单克隆抗体对CD8 + 细胞进行预防性体内清除,与对照组相比导致疾病发作更早,表明CD8 + 细胞调节关节炎的发展。通过V65单克隆抗体对γδ T细胞进行体内清除并未改变疾病进程,表明具有疾病抑制作用的CD8 + 细胞是αβ T细胞或NK细胞。