TIM1 is an endogenous ligand for LMIR5/CD300b: LMIR5 deficiency ameliorates mouse kidney ischemia/reperfusion injury.
TIM1 is an endogenous ligand for LMIR5/CD300b: LMIR5 deficiency ameliorates mouse kidney ischemia/reperfusion injury.
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DOI：
10.1084/jem.20090581
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发表时间：
2010-07-05
期刊：
影响因子：
--
通讯作者：
Kitamura T
中科院分区：
文献类型：
--
作者：
Yamanishi Y;Kitaura J;Izawa K;Kaitani A;Komeno Y;Nakamura M;Yamazaki S;Enomoto Y;Oki T;Akiba H;Abe T;Komori T;Morikawa Y;Kiyonari H;Takai T;Okumura K;Kitamura T
白细胞单免疫球蛋白（IG）样受体5（LMIR 5）/CD 300 b是一种主要在骨髓细胞中表达的DAP 12偶联活化受体。LMIR的配体未见报道。我们已经确定了T细胞IG粘蛋白1（TIM 1）作为一个可能的配体LMIR 5的逆转录病毒介导的表达克隆。在LMIR家族中，TIM 1仅与LMIR 5相互作用，而LMIR 5与TIM 4以及TIM 1相互作用。LMIR 5的免疫球蛋白样结构域在TIM 1的免疫球蛋白样结构域内的磷脂酰丝氨酸（PS）结合位点附近与TIM 1结合。与TIM 1或TIM 4的结合不同，LMIR 5不能与PS结合。LMIR 5结合不影响TIM 1或TIM 4介导的凋亡细胞的吞噬作用，并且用TIM 1或TIM 4刺激诱导LMIR 5介导的肥大细胞活化。值得注意的是，LMIR 5缺乏抑制了背侧气囊中TIM 1-Fc诱导的中性粒细胞募集，并且LMIR 5缺乏减弱了TIM 1表达上调的肾脏缺血/再灌注损伤模型中的中性粒细胞积聚。在该模型中，LMIR 5缺乏导致急性期肾小管坏死和管型形成改善。总的来说，我们的结果表明，TIM 1是LMIR 5的内源性配体，并且TIM 1-LMIR 5相互作用在骨髓细胞的免疫调节中起生理作用。
Leukocyte mono-immunoglobulin (Ig)–like receptor 5 (LMIR5)/CD300b is a DAP12-coupled activating receptor predominantly expressed in myeloid cells. The ligands for LMIR have not been reported. We have identified T cell Ig mucin 1 (TIM1) as a possible ligand for LMIR5 by retrovirus-mediated expression cloning. TIM1 interacted only with LMIR5 among the LMIR family, whereas LMIR5 interacted with TIM4 as well as TIM1. The Ig-like domain of LMIR5 bound to TIM1 in the vicinity of the phosphatidylserine (PS)-binding site within the Ig-like domain of TIM1. Unlike its binding to TIM1 or TIM4, LMIR5 failed to bind to PS. LMIR5 binding did not affect TIM1- or TIM4-mediated phagocytosis of apoptotic cells, and stimulation with TIM1 or TIM4 induced LMIR5-mediated activation of mast cells. Notably, LMIR5 deficiency suppressed TIM1-Fc–induced recruitment of neutrophils in the dorsal air pouch, and LMIR5 deficiency attenuated neutrophil accumulation in a model of ischemia/reperfusion injury in the kidneys in which TIM1 expression is up-regulated. In that model, LMIR5 deficiency resulted in ameliorated tubular necrosis and cast formation in the acute phase. Collectively, our results indicate that TIM1 is an endogenous ligand for LMIR5 and that the TIM1–LMIR5 interaction plays a physiological role in immune regulation by myeloid cells.
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