Smith Sarah A, Samokhin Andriy O, Alfadi Mabruka, Murphy Emer C, Rhodes David, Holcombe W Mike L, Kiss-Toth Endre, Storey Robert F, Yee Siu-Pok, Francis Sheila E, Qwarnstrom Eva E
Department of Infection, Immunity & Cardiovascular Disease, University of Sheffield, Sheffield, United Kingdom.
Department of Computer Science, University of Sheffield, Sheffield, United Kingdom.
JACC Basic Transl Sci. 2017 Aug 28;2(4):398-414. doi: 10.1016/j.jacbts.2017.03.014. eCollection 2017 Aug.
Expression of the interleukin-1 receptor type I (IL-1RI) co-receptor Toll-like and interleukin-1 receptor regulator (TILRR) is significantly increased in blood monocytes following myocardial infarction and in the atherosclerotic plaque, whereas levels in healthy tissue are low. TILRR association with IL-1RI at these sites causes aberrant activation of inflammatory genes, which underlie progression of cardiovascular disease. The authors show that genetic deletion of TILRR or antibody blocking of TILRR function reduces development of atherosclerotic plaques. Lesions exhibit decreased levels of monocytes, with increases in collagen and smooth muscle cells, characteristic features of stable plaques. The results suggest that TILRR may constitute a rational target for site- and signal-specific inhibition of vascular disease.
心肌梗死后血液单核细胞以及动脉粥样硬化斑块中，白细胞介素-1Ⅰ型受体（IL-1RI）共受体Toll样和白细胞介素-1受体调节剂（TILRR）的表达显著增加，而健康组织中的水平较低。在这些部位，TILRR与IL-1RI的结合会导致炎症基因异常激活，这是心血管疾病进展的基础。作者表明，TILRR的基因缺失或TILRR功能的抗体阻断可减少动脉粥样硬化斑块的形成。病变部位单核细胞水平降低，胶原蛋白和平滑肌细胞增加，这是稳定斑块的特征。结果表明，TILRR可能是血管疾病位点和信号特异性抑制的合理靶点。
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