Analysis of mouse LMIR5/CLM-7 as an activating receptor

Differential regulation of LMIR5/CLM-7 in mouse versus human cells

Yoshinori Yamanishi, Jiro Kitaura, Kumi Izawa, Takayuki Matsuoka, Toshihiko Oki, Yang Lu, Fumi Shibata, Satoshi Yamazaki, Hidetoshi Kumagai, Hideaki Nakajima, Mari Maeda-Yamamoto, Victor L J Tybulewicz, Toshiyuki Takai, Toshio Kitamura

Research output: Contribution to journalArticle

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Abstract

We have analyzed leukocyte mono-Ig-like receptor 5 (LMIR5) as an activating receptor among paired LMIRs. Mouse LMIR5 (mLMIR5) is expressed in myeloid cells such as mast cells, granulocytes, macrophages, and dendritic cells. Cross-linking of transduced mLMIR5 in bone marrow-derived mast cells (BMMCs) caused activation events, including cytokine production, cell survival, degranulation, and adhesion to the extracellular matrix. mLMIR5 associated with DAP12 and to a lesser extent with DAP10, and mLMIR5-mediated functions of BMMCs were strongly inhibited by DAP12 deficiency. Importantly, cross-linking of endogenous mLMIR5 induced Syk-dependent activation of fetal liver-derived mast cells. Unlike mLMIR5, cross-linking of human LMIR5 (hLMIR5) induced cytokine production of BMMCs even in the absence of both DAP12 and DAP10, suggesting the existence of unidentified adaptors. Interestingly, hLMIR5 possessed a tyrosine residue (Y188) in the cytoplasmic region. Signaling via Y188 phosphorylation played a predominant role in hLMIR5-mediated cytokine production in DAP12-deficient, but not wildtype BMMCs. In addition, experiments using DAP10/DAP12 double-deficient BMMCs suggested the existence of Y188 phoshorylation-dependent and -independent signals from unidentified adaptors. Collectively, although both mouse and human LMIR5 play activatory roles in innate immunity cells, the functions of LMIR5 were differentially regulated in mouse versus human cells.

Original languageEnglish
Pages (from-to)688-698
Number of pages11
JournalBlood
Volume111
Issue number2
DOIs
Publication statusPublished - 2008 Jan 15
Externally publishedYes

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Mast Cells
Bone
Leukocytes
Cells
Bone Marrow
Cytokines
Chemical activation
Phosphorylation
Macrophages
Liver
Cell Degranulation
Tyrosine
Adhesion
Myeloid Cells
mouse LMIR5 protein
Granulocytes
Innate Immunity
Cell Adhesion
Dendritic Cells
Extracellular Matrix

ASJC Scopus subject areas

  • Hematology

Cite this

Yamanishi, Y., Kitaura, J., Izawa, K., Matsuoka, T., Oki, T., Lu, Y., ... Kitamura, T. (2008). Analysis of mouse LMIR5/CLM-7 as an activating receptor: Differential regulation of LMIR5/CLM-7 in mouse versus human cells. Blood, 111(2), 688-698. https://doi.org/10.1182/blood-2007-04-085787

Analysis of mouse LMIR5/CLM-7 as an activating receptor : Differential regulation of LMIR5/CLM-7 in mouse versus human cells. / Yamanishi, Yoshinori; Kitaura, Jiro; Izawa, Kumi; Matsuoka, Takayuki; Oki, Toshihiko; Lu, Yang; Shibata, Fumi; Yamazaki, Satoshi; Kumagai, Hidetoshi; Nakajima, Hideaki; Maeda-Yamamoto, Mari; Tybulewicz, Victor L J; Takai, Toshiyuki; Kitamura, Toshio.

In: Blood, Vol. 111, No. 2, 15.01.2008, p. 688-698.

Research output: Contribution to journalArticle

Yamanishi, Y, Kitaura, J, Izawa, K, Matsuoka, T, Oki, T, Lu, Y, Shibata, F, Yamazaki, S, Kumagai, H, Nakajima, H, Maeda-Yamamoto, M, Tybulewicz, VLJ, Takai, T & Kitamura, T 2008, 'Analysis of mouse LMIR5/CLM-7 as an activating receptor: Differential regulation of LMIR5/CLM-7 in mouse versus human cells', Blood, vol. 111, no. 2, pp. 688-698. https://doi.org/10.1182/blood-2007-04-085787
Yamanishi, Yoshinori ; Kitaura, Jiro ; Izawa, Kumi ; Matsuoka, Takayuki ; Oki, Toshihiko ; Lu, Yang ; Shibata, Fumi ; Yamazaki, Satoshi ; Kumagai, Hidetoshi ; Nakajima, Hideaki ; Maeda-Yamamoto, Mari ; Tybulewicz, Victor L J ; Takai, Toshiyuki ; Kitamura, Toshio. / Analysis of mouse LMIR5/CLM-7 as an activating receptor : Differential regulation of LMIR5/CLM-7 in mouse versus human cells. In: Blood. 2008 ; Vol. 111, No. 2. pp. 688-698.
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abstract = "We have analyzed leukocyte mono-Ig-like receptor 5 (LMIR5) as an activating receptor among paired LMIRs. Mouse LMIR5 (mLMIR5) is expressed in myeloid cells such as mast cells, granulocytes, macrophages, and dendritic cells. Cross-linking of transduced mLMIR5 in bone marrow-derived mast cells (BMMCs) caused activation events, including cytokine production, cell survival, degranulation, and adhesion to the extracellular matrix. mLMIR5 associated with DAP12 and to a lesser extent with DAP10, and mLMIR5-mediated functions of BMMCs were strongly inhibited by DAP12 deficiency. Importantly, cross-linking of endogenous mLMIR5 induced Syk-dependent activation of fetal liver-derived mast cells. Unlike mLMIR5, cross-linking of human LMIR5 (hLMIR5) induced cytokine production of BMMCs even in the absence of both DAP12 and DAP10, suggesting the existence of unidentified adaptors. Interestingly, hLMIR5 possessed a tyrosine residue (Y188) in the cytoplasmic region. Signaling via Y188 phosphorylation played a predominant role in hLMIR5-mediated cytokine production in DAP12-deficient, but not wildtype BMMCs. In addition, experiments using DAP10/DAP12 double-deficient BMMCs suggested the existence of Y188 phoshorylation-dependent and -independent signals from unidentified adaptors. Collectively, although both mouse and human LMIR5 play activatory roles in innate immunity cells, the functions of LMIR5 were differentially regulated in mouse versus human cells.",
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T2 - Differential regulation of LMIR5/CLM-7 in mouse versus human cells

AU - Yamanishi, Yoshinori

AU - Kitaura, Jiro

AU - Izawa, Kumi

AU - Matsuoka, Takayuki

AU - Oki, Toshihiko

AU - Lu, Yang

AU - Shibata, Fumi

AU - Yamazaki, Satoshi

AU - Kumagai, Hidetoshi

AU - Nakajima, Hideaki

AU - Maeda-Yamamoto, Mari

AU - Tybulewicz, Victor L J

AU - Takai, Toshiyuki

AU - Kitamura, Toshio

PY - 2008/1/15

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N2 - We have analyzed leukocyte mono-Ig-like receptor 5 (LMIR5) as an activating receptor among paired LMIRs. Mouse LMIR5 (mLMIR5) is expressed in myeloid cells such as mast cells, granulocytes, macrophages, and dendritic cells. Cross-linking of transduced mLMIR5 in bone marrow-derived mast cells (BMMCs) caused activation events, including cytokine production, cell survival, degranulation, and adhesion to the extracellular matrix. mLMIR5 associated with DAP12 and to a lesser extent with DAP10, and mLMIR5-mediated functions of BMMCs were strongly inhibited by DAP12 deficiency. Importantly, cross-linking of endogenous mLMIR5 induced Syk-dependent activation of fetal liver-derived mast cells. Unlike mLMIR5, cross-linking of human LMIR5 (hLMIR5) induced cytokine production of BMMCs even in the absence of both DAP12 and DAP10, suggesting the existence of unidentified adaptors. Interestingly, hLMIR5 possessed a tyrosine residue (Y188) in the cytoplasmic region. Signaling via Y188 phosphorylation played a predominant role in hLMIR5-mediated cytokine production in DAP12-deficient, but not wildtype BMMCs. In addition, experiments using DAP10/DAP12 double-deficient BMMCs suggested the existence of Y188 phoshorylation-dependent and -independent signals from unidentified adaptors. Collectively, although both mouse and human LMIR5 play activatory roles in innate immunity cells, the functions of LMIR5 were differentially regulated in mouse versus human cells.

AB - We have analyzed leukocyte mono-Ig-like receptor 5 (LMIR5) as an activating receptor among paired LMIRs. Mouse LMIR5 (mLMIR5) is expressed in myeloid cells such as mast cells, granulocytes, macrophages, and dendritic cells. Cross-linking of transduced mLMIR5 in bone marrow-derived mast cells (BMMCs) caused activation events, including cytokine production, cell survival, degranulation, and adhesion to the extracellular matrix. mLMIR5 associated with DAP12 and to a lesser extent with DAP10, and mLMIR5-mediated functions of BMMCs were strongly inhibited by DAP12 deficiency. Importantly, cross-linking of endogenous mLMIR5 induced Syk-dependent activation of fetal liver-derived mast cells. Unlike mLMIR5, cross-linking of human LMIR5 (hLMIR5) induced cytokine production of BMMCs even in the absence of both DAP12 and DAP10, suggesting the existence of unidentified adaptors. Interestingly, hLMIR5 possessed a tyrosine residue (Y188) in the cytoplasmic region. Signaling via Y188 phosphorylation played a predominant role in hLMIR5-mediated cytokine production in DAP12-deficient, but not wildtype BMMCs. In addition, experiments using DAP10/DAP12 double-deficient BMMCs suggested the existence of Y188 phoshorylation-dependent and -independent signals from unidentified adaptors. Collectively, although both mouse and human LMIR5 play activatory roles in innate immunity cells, the functions of LMIR5 were differentially regulated in mouse versus human cells.

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