Cellular autoreactivity against heat shock protein 60 in renal transplant patients: peripheral and graft-infiltrating responses
Cellular autoreactivity against heat shock protein 60 in renal transplant patients: peripheral and graft-infiltrating responses
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DOI：
10.1111/j.1365-2249.2006.03195.x
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发表时间：
2006-10-01
影响因子：
4.6
通讯作者：
Coelho, V.
中科院分区：
文献类型：
--
作者：
Caldas, C.;Luna, E.;Coelho, V.
热休克蛋白 60 (Hsp60) 的自身反应性与慢性炎症的发病机制和调节有关，尤其是自身免疫性疾病。在移植中，缺乏关于识别自身 Hsp60 的细胞的细胞因子谱和特异性以及移植后自身反应动力学的信息。我们研究了肾移植患者外周血和移植物浸润淋巴细胞对 Hsp60 的细胞反应性。外周血单核细胞中该蛋白诱导的细胞因子产生表明，在移植后后期，白细胞介素 (IL)-10 占主导地位，主要是对中间肽和 C 末端肽的反应。与长期临床稳定的患者相比，慢性排斥患者对 Hsp60 表现出较高的 IL-10/干扰素 (IFN)-gamma 比值反应性。与抗原呈递细胞共培养的移植物浸润 T 细胞系在 Hsp60 刺激后优先产生 IL-10。这些结果表明，除了其促炎活性之外，移植中对 Hsp60 的自身反应也可能具有调节作用。
Autoreactivity to heat shock protein 60 (Hsp60) has been implicated in the pathogenesis and regulation of chronic inflammation, especially in autoimmune diseases. In transplantation, there is a lack of information regarding the cytokine profile and specificity of cells that recognize self-Hsp60 as well as the kinetics of autoreactivity following transplantation. We studied the cellular reactivity of peripheral and graft-infiltrating lymphocytes against Hsp60 in renal transplant patients. Cytokine production induced by this protein in peripheral blood mononuclear cells indicated a predominance of interleukin (IL)-10 during the late post-transplantation period, mainly in response to intermediate and C-terminal peptides. Patients with chronic rejection presented reactivity to Hsp60 with a higher IL-10/interferon (IFN)-gamma ratio compared to long-term clinically stable patients. Graft-infiltrating T cell lines, cocultured with antigen-presenting cells, preferentially produced IL-10 after Hsp60 stimulation. These results suggest that, besides its proinflammatory activity, autoreactivity to Hsp60 in transplantation may also have a regulatory role.