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TIM1 is an endogenous ligand for LMIR5/CD300b: LMIR5 deficiency ameliorates mouse kidney ischemia/reperfusion injury
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...
Autores principales: | , , , , , , , , , , , , , , , , |
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Formato: | Texto |
Lenguaje: | English |
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The Rockefeller University Press
2010
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2901072/ https://www.ncbi.nlm.nih.gov/pubmed/20566714 http://dx.doi.org/10.1084/jem.20090581 |
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author | Yamanishi, Yoshinori Kitaura, Jiro Izawa, Kumi Kaitani, Ayako Komeno, Yukiko Nakamura, Masaki Yamazaki, Satoshi Enomoto, Yutaka Oki, Toshihiko Akiba, Hisaya Abe, Takaya Komori, Tadasuke Morikawa, Yoshihiro Kiyonari, Hiroshi Takai, Toshiyuki Okumura, Ko Kitamura, Toshio |
author_facet | Yamanishi, Yoshinori Kitaura, Jiro Izawa, Kumi Kaitani, Ayako Komeno, Yukiko Nakamura, Masaki Yamazaki, Satoshi Enomoto, Yutaka Oki, Toshihiko Akiba, Hisaya Abe, Takaya Komori, Tadasuke Morikawa, Yoshihiro Kiyonari, Hiroshi Takai, Toshiyuki Okumura, Ko Kitamura, Toshio |
author_sort | Yamanishi, Yoshinori |
collection | PubMed |
description | 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. |
format | Text |
id | pubmed-2901072 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2010 |
publisher | The Rockefeller University Press |
record_format | MEDLINE/PubMed |
spelling | pubmed-29010722011-01-05 TIM1 is an endogenous ligand for LMIR5/CD300b: LMIR5 deficiency ameliorates mouse kidney ischemia/reperfusion injury Yamanishi, Yoshinori Kitaura, Jiro Izawa, Kumi Kaitani, Ayako Komeno, Yukiko Nakamura, Masaki Yamazaki, Satoshi Enomoto, Yutaka Oki, Toshihiko Akiba, Hisaya Abe, Takaya Komori, Tadasuke Morikawa, Yoshihiro Kiyonari, Hiroshi Takai, Toshiyuki Okumura, Ko Kitamura, Toshio J Exp Med Article 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. The Rockefeller University Press 2010-07-05 /pmc/articles/PMC2901072/ /pubmed/20566714 http://dx.doi.org/10.1084/jem.20090581 Text en © 2010 Yamanishi et al. This article is distributed under the terms of an Attribution–Noncommercial–Share Alike–No Mirror Sites license for the first six months after the publication date (see http://www.rupress.org/terms). After six months it is available under a Creative Commons License (Attribution–Noncommercial–Share Alike 3.0 Unported license, as described at http://creativecommons.org/licenses/by-nc-sa/3.0/). |
spellingShingle | Article Yamanishi, Yoshinori Kitaura, Jiro Izawa, Kumi Kaitani, Ayako Komeno, Yukiko Nakamura, Masaki Yamazaki, Satoshi Enomoto, Yutaka Oki, Toshihiko Akiba, Hisaya Abe, Takaya Komori, Tadasuke Morikawa, Yoshihiro Kiyonari, Hiroshi Takai, Toshiyuki Okumura, Ko Kitamura, Toshio TIM1 is an endogenous ligand for LMIR5/CD300b: LMIR5 deficiency ameliorates mouse kidney ischemia/reperfusion injury |
title | TIM1 is an endogenous ligand for LMIR5/CD300b: LMIR5 deficiency ameliorates mouse kidney ischemia/reperfusion injury |
title_full | TIM1 is an endogenous ligand for LMIR5/CD300b: LMIR5 deficiency ameliorates mouse kidney ischemia/reperfusion injury |
title_fullStr | TIM1 is an endogenous ligand for LMIR5/CD300b: LMIR5 deficiency ameliorates mouse kidney ischemia/reperfusion injury |
title_full_unstemmed | TIM1 is an endogenous ligand for LMIR5/CD300b: LMIR5 deficiency ameliorates mouse kidney ischemia/reperfusion injury |
title_short | TIM1 is an endogenous ligand for LMIR5/CD300b: LMIR5 deficiency ameliorates mouse kidney ischemia/reperfusion injury |
title_sort | tim1 is an endogenous ligand for lmir5/cd300b: lmir5 deficiency ameliorates mouse kidney ischemia/reperfusion injury |
topic | Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2901072/ https://www.ncbi.nlm.nih.gov/pubmed/20566714 http://dx.doi.org/10.1084/jem.20090581 |
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