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Comparative analysis of Annexin A1-formyl peptide receptor 2/ALX expression in human leukocyte subsets
Recent studies have associated the dysregulated expression of Annexin-A1/Formyl peptide receptor 2 (FPR2/ALX) system with the development of autoimmune diseases. In this study we systematically scanned human leukocyte subsets for the presence of this pathway aiming to provide a roadmap that will hel...
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Published in: | International immunopharmacology 2011, Vol.11 (1), p.55-66 |
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Main Authors: | , , , , , |
Format: | Article |
Language: | English |
Subjects: | |
Citations: | Items that this one cites Items that cite this one |
Online Access: | Get full text |
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Summary: | Recent studies have associated the dysregulated expression of Annexin-A1/Formyl peptide receptor 2 (FPR2/ALX) system with the development of autoimmune diseases. In this study we systematically scanned human leukocyte subsets for the presence of this pathway aiming to provide a roadmap that will help investigators to explore possible links between the development of immune related disorders and the expression of this system. Our results show that neutrophils, monocytes and NK cells express higher levels of both AnxA1 and FPR2/ALX compared to T or B cells. Further analysis of specific T cell subsets revealed higher levels in activated CD25
+ and memory CD45RO CD4 T cells compared to resting CD25
− or naïve CD45RA CD4 T cells. Together the results expand our knowledge of the AnxA1-FPR2/ALX system in immune cells and provide new avenues for investigation into the functions of this signalling pathway in systems other than that classically described for neutrophils.
►This is the first study showing FPR2/ALX as the genuine receptor for full-length Annexin-A1. ►This study demonstrated that Annexin-A1 modulates the strength of TCR signalling. ►A comprehensive review of the biological functions of formyl peptide receptors. ►This study provided the first evidence of Annexin-A1-derived peptides as ligand for formyl peptide receptors. |
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ISSN: | 1567-5769 1878-1705 |
DOI: | 10.1016/j.intimp.2010.10.006 |