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Cellular and humoral reactivity pattern to the mycobacterial heat shock protein hsp65 in pristane induced arthritis susceptible and hsp65 protected DBA/1 mice.

作者信息

Thompson S J, Hitsumoto Y, Ghoraishian M, van der Zee R, Elson C J

机构信息

Department of Pathology and Microbiology, School of Medical Sciences, University of Bristol, UK.

出版信息

Autoimmunity. 1991;11(2):89-95. doi: 10.3109/08916939109035139.

DOI:10.3109/08916939109035139
PMID:1669738
Abstract

We have analysed the cellular and humoral immunity to the mycobacterial 65 kD heat shock protein (hsp65) in groups of DBA/1 mice with arthritis induced by intraperitoneal injection of the mineral oil pristane. Here we confirm that DBA/1 mice are highly susceptible to pristane induced arthritis (PIA) and demonstrate that the incidence of arthritis can be modulated by either pretreatment with low dose irradiation or by preimmunisation with recombinant hsp65. Global cellular responses to antigens such as BSA or type II collagen were not enhanced or impaired within groups of arthritic (A) or non-arthritic (NA) mice. However, the cellular response to hsp65 in arthritic animals preimmunised with the 65 kD antigen was significantly elevated in comparison to hsp65 preimmunised mice that were resistant to the induction of disease. On the contrary, the level of hsp65 specific antibodies was much high in NA animals than in PIA mice. CBA/Igb mice are partially susceptible to the induction of PIA. We have previously reported that arthritic CBA/Igb mice have both elevated cellular and humoral reactivity to hsp65. Although a central pivotal role for hsp65 has been postulated in autoimmune diseases these results indicate that there is no simple relationship between the pathogenesis of PIA and immune responses to hsp65.

摘要

相似文献

1
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2
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引用本文的文献

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The involvement of heat-shock proteins in the pathogenesis of autoimmune arthritis: a critical appraisal.热休克蛋白在自身免疫性关节炎发病机制中的作用:批判性评价。
Semin Arthritis Rheum. 2010 Oct;40(2):164-75. doi: 10.1016/j.semarthrit.2009.10.002. Epub 2009 Dec 6.
2
The route of administration of an immunodominant peptide derived from heat-shock protein 65 dramatically affects disease outcome in pristane-induced arthritis.源自热休克蛋白65的免疫显性肽的给药途径显著影响 pristane 诱导的关节炎的疾病结局。
Immunology. 2000 Mar;99(3):338-44. doi: 10.1046/j.1365-2567.2000.00969.x.
3
Pristane-induced arthritis is CD4+ T-cell dependent.
pristane诱导的关节炎依赖于CD4 + T细胞
Immunology. 1997 Jan;90(1):81-6. doi: 10.1046/j.1365-2567.1997.00121.x.
4
B- and T-cell autoantigens in pristane-induced arthritis.
Immunology. 1996 Oct;89(2):189-94. doi: 10.1046/j.1365-2567.1996.d01-730.x.
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Molecular chaperones and disease.分子伴侣与疾病
Inflamm Res. 1996 Apr;45(4):155-8. doi: 10.1007/BF02285154.
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7
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