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Activation of natural killer cells and dendritic cells upon recognition of a novel CD99-like ligand by paired immunoglobulin-like type 2 receptor.

Shiratori I, Ogasawara K, Saito T, Lanier LL, Arase H - J. Exp. Med. (2004)

Bottom Line: Transcripts of PILR ligand are present in many tissues, including some T cell lines.Cells expressing the PILR ligand specifically activated NK cells and dendritic cells that express the activating PILRbeta.Our findings reveal a new regulatory mechanism of innate immunity by PILR and its CD99-like ligand.

View Article: PubMed Central - PubMed

Affiliation: Department of Molecular Genetics, Chiba University Graduate School of Medicine, 1-8-1 Inohana, Chuoku, 260-8670, Japan.

ABSTRACT
Paired receptors that consist of highly related activating and inhibitory receptors are widely involved in the regulation of the immune system. Here, we report a mouse orthologue of the human activating paired immunoglobulin-like type 2 receptor (PILR) beta, which was cloned from a cDNA library of natural killer (NK) cells based on its ability to associate with the DAP12 signaling adaptor protein. The activating PILRbeta was expressed not only on NK cells but also on dendritic cells and macrophages. Furthermore, we have identified a novel CD99-like molecule as a ligand for the activating PILRbeta and inhibitory PILRalpha receptors. Transcripts of PILR ligand are present in many tissues, including some T cell lines. Cells expressing the PILR ligand specifically activated NK cells and dendritic cells that express the activating PILRbeta. Our findings reveal a new regulatory mechanism of innate immunity by PILR and its CD99-like ligand.

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Transcription of PILR-L in various tissues. Transcription of PILRα and PILRβ in various tissues was analyzed by real-time quantitative RT-PCR. Transcription of β-actin was used as a standard and relative expression levels of PILR-L to the amounts present in spleen are shown. S. intestine, small intestine.
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fig6: Transcription of PILR-L in various tissues. Transcription of PILRα and PILRβ in various tissues was analyzed by real-time quantitative RT-PCR. Transcription of β-actin was used as a standard and relative expression levels of PILR-L to the amounts present in spleen are shown. S. intestine, small intestine.

Mentions: When the PILR-L was transfected into Ba/F3 cells or 293T cells, the transfectants were stained well with PILRβ-Ig (Fig. 5 B). Furthermore, these PILR-L transfectants were also stained with PILRα-Ig. This indicated that PILR-L is a ligand for both PILRα and PILRβ. Indeed, when PILR-L was precipitated from cell lysates of PILR-L–transfected Ba/F3 cells using PILRα-Ig and PILRβ-Ig, PILR-L was clearly detected as a 17-kD molecule, although PILRβ-Ig precipitated much less PILR-L. A control Ig did not precipitate the 17-kD protein, and this protein was not immunoprecipitated from untransfected Ba/F3 cells (Fig. 5 C). The actual molecular weight was the same as the predicted molecular weight of PILR-L based on the deduced amino acid sequence. We analyzed the expression of PILR-L transcripts by real-time quantitative PCR. PILR-L transcripts were present in most tissues, and expressions of PILR-L were relatively high in lung, spleen, thymus, liver, and spinal cord (Fig. 6).


Activation of natural killer cells and dendritic cells upon recognition of a novel CD99-like ligand by paired immunoglobulin-like type 2 receptor.

Shiratori I, Ogasawara K, Saito T, Lanier LL, Arase H - J. Exp. Med. (2004)

Transcription of PILR-L in various tissues. Transcription of PILRα and PILRβ in various tissues was analyzed by real-time quantitative RT-PCR. Transcription of β-actin was used as a standard and relative expression levels of PILR-L to the amounts present in spleen are shown. S. intestine, small intestine.
© Copyright Policy
Related In: Results  -  Collection

Show All Figures
getmorefigures.php?uid=PMC2211832&req=5

fig6: Transcription of PILR-L in various tissues. Transcription of PILRα and PILRβ in various tissues was analyzed by real-time quantitative RT-PCR. Transcription of β-actin was used as a standard and relative expression levels of PILR-L to the amounts present in spleen are shown. S. intestine, small intestine.
Mentions: When the PILR-L was transfected into Ba/F3 cells or 293T cells, the transfectants were stained well with PILRβ-Ig (Fig. 5 B). Furthermore, these PILR-L transfectants were also stained with PILRα-Ig. This indicated that PILR-L is a ligand for both PILRα and PILRβ. Indeed, when PILR-L was precipitated from cell lysates of PILR-L–transfected Ba/F3 cells using PILRα-Ig and PILRβ-Ig, PILR-L was clearly detected as a 17-kD molecule, although PILRβ-Ig precipitated much less PILR-L. A control Ig did not precipitate the 17-kD protein, and this protein was not immunoprecipitated from untransfected Ba/F3 cells (Fig. 5 C). The actual molecular weight was the same as the predicted molecular weight of PILR-L based on the deduced amino acid sequence. We analyzed the expression of PILR-L transcripts by real-time quantitative PCR. PILR-L transcripts were present in most tissues, and expressions of PILR-L were relatively high in lung, spleen, thymus, liver, and spinal cord (Fig. 6).

Bottom Line: Transcripts of PILR ligand are present in many tissues, including some T cell lines.Cells expressing the PILR ligand specifically activated NK cells and dendritic cells that express the activating PILRbeta.Our findings reveal a new regulatory mechanism of innate immunity by PILR and its CD99-like ligand.

View Article: PubMed Central - PubMed

Affiliation: Department of Molecular Genetics, Chiba University Graduate School of Medicine, 1-8-1 Inohana, Chuoku, 260-8670, Japan.

ABSTRACT
Paired receptors that consist of highly related activating and inhibitory receptors are widely involved in the regulation of the immune system. Here, we report a mouse orthologue of the human activating paired immunoglobulin-like type 2 receptor (PILR) beta, which was cloned from a cDNA library of natural killer (NK) cells based on its ability to associate with the DAP12 signaling adaptor protein. The activating PILRbeta was expressed not only on NK cells but also on dendritic cells and macrophages. Furthermore, we have identified a novel CD99-like molecule as a ligand for the activating PILRbeta and inhibitory PILRalpha receptors. Transcripts of PILR ligand are present in many tissues, including some T cell lines. Cells expressing the PILR ligand specifically activated NK cells and dendritic cells that express the activating PILRbeta. Our findings reveal a new regulatory mechanism of innate immunity by PILR and its CD99-like ligand.

Show MeSH