Kumar Chauhan S, Kumar Tripathy N, Sinha N, Singh M, Nityanand S
Department of Haematology, Sanjay Gandhi Post Graduate Institute of Medical Sciences, Lucknow, India.
Clin Exp Immunol. 2004 Dec;138(3):547-53. doi: 10.1111/j.1365-2249.2004.02644.x.
Expression of heat shock protein (HSP)-65 as well as infiltration of T-cells in arterial lesions and raised levels of circulating antibodies against mycobacterial HSP65 (mHSP65) led us to the concept that mHSP65 or its human homologue (hHSP60) might be involved in the etiopathogenesis of Takayasu's arteritis (TA). Therefore, we investigated mHSP65 and hHSP60 reactive peripheral blood T-cell subsets by BrdU incorporation assay and flow cytometry as well as investigating the different isotypes of anti-mHSP65 and hHSP60 antibodies by ELISA. Eighty-four percent (22/26) of the TA patients were observed to show T-cell proliferation to mHSP65 and hHSP60 whereas only 16% (3/18) healthy controls showed such proliferation (P <0.001). Both HSPs induced proliferation of exclusively CD4+ T-cells and not CD8+ T-cells. We also observed a significantly higher prevalence of only the IgG isotype reactive to mHSP65 and hHSP60 in TA as compared to HC (mHSP65: 92% TA versus 11% HC, P <0.0001 and hHSP60: 84% versus 22%, P <0.001). Our data show a significant correlation between mHSP65 and hHSP60 reactive T-cells (CD3+: r=0.901; CD4+: r=0.968) as well as anti-mHSP65 and anti-hHSP60 IgG antibodies (r=0.814) suggesting an infection induced autoimmunity in TA, possibly induced by molecular mimicry between mHSP65 and hHSP60 or other tissue specific antigens.
热休克蛋白（HSP）-65的表达、动脉病变中T细胞的浸润以及循环中抗分枝杆菌HSP65（mHSP65）抗体水平的升高，使我们想到mHSP65或其人类同源物（hHSP60）可能参与了高安动脉炎（TA）的发病机制。因此，我们通过BrdU掺入试验和流式细胞术研究了对mHSP65和hHSP60有反应的外周血T细胞亚群，并通过ELISA研究了抗mHSP65和hHSP60抗体的不同亚型。观察到84%（22/26）的TA患者对mHSP65和hHSP60表现出T细胞增殖，而只有16%（3/18）的健康对照有这种增殖（P<0.001）。两种热休克蛋白均仅诱导CD4+T细胞增殖，而非CD8+T细胞。我们还观察到，与健康对照相比，TA患者中仅对mHSP65和hHSP60有反应的IgG亚型的患病率显著更高（mHSP65：TA患者为92%，健康对照为11%，P<0.0001；hHSP60：84%对22%，P<0.001）。我们的数据显示，对mHSP65和hHSP60有反应的T细胞（CD3+：r=0.901；CD4+：r=0.968）以及抗mHSP65和抗hHSP60 IgG抗体（r=0.814）之间存在显著相关性，提示TA中存在感染诱导的自身免疫，可能是由mHSP65和hHSP60或其他组织特异性抗原之间的分子模拟诱导的。
