Counter-regulation of the ligand-receptor pair Leda-1/Pianp and Pilrα during the LPS-mediated immune response of murine macrophages
Liver endothelial differentiation-associated protein-1 (Leda-1/Pianp) is a type-I-transmembrane protein that is able to bind and activate immune inhibitory receptor Pilrα. Here we show that Leda-1/Pianp is strain-specifically expressed in lymphoid organs and macrophages of Th2-prone BALB/c mice but...
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| Hauptverfasser: | , , , , , , |
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| Dokumenttyp: | Article (Journal) |
| Sprache: | Englisch |
| Veröffentlicht: |
4 September 2015
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| In: |
Biochemical and biophysical research communications
Year: 2015, Jahrgang: 464, Heft: 4, Pages: 1078-1083 |
| ISSN: | 1090-2104 |
| DOI: | 10.1016/j.bbrc.2015.07.079 |
| Online-Zugang: | Verlag, Volltext: http://dx.doi.org/10.1016/j.bbrc.2015.07.079 Verlag, Volltext: http://www.sciencedirect.com/science/article/pii/S0006291X15303090 |
| Verfasserangaben: | Siladitta Biswas, Monica Adrian, Konstantin Evdokimov, Kai Schledzewski, Jochen Weber, Manuel Winkler, Sergij Goerdt, Cyrill Géraud |
| Zusammenfassung: | Liver endothelial differentiation-associated protein-1 (Leda-1/Pianp) is a type-I-transmembrane protein that is able to bind and activate immune inhibitory receptor Pilrα. Here we show that Leda-1/Pianp is strain-specifically expressed in lymphoid organs and macrophages of Th2-prone BALB/c mice but not of Th1-prone C57BL/6J mice. LPS stimulation of BALB/c bone marrow-derived macrophages (BMM) and macrophage-like Raw 264.7 cells conversely regulated Leda-1/Pianp and Pilrα expression. Pilrα induction was caused by LPS-mediated transcriptional modulation and increased mRNA expression. On the other hand, the LPS-mediated decline of Leda-1/Pianp expression was the result of proteolytic degradation by matrix metalloproteinases. In summary, these findings demonstrate that counter-regulation of the ligand-receptor pair Leda-1/Pianp and Pilrα is part of the complex innate immune response of macrophages and its genetically determined strain-specific modulation. |
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| Beschreibung: | Gesehen am 22.03.2018 |
| Beschreibung: | Online Resource |
| ISSN: | 1090-2104 |
| DOI: | 10.1016/j.bbrc.2015.07.079 |