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Allergy. 2011 Feb;66(2):155-62. doi: 10.1111/j.1398-9995.2010.02458.x. Epub 2010 Aug 17.

Role of PD-L1 and PD-L2 in allergic diseases and asthma.

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  • 1Department of Molecular Microbiology and Immunology, Keck School of Medicine, University of Southern California, 1450 Biggy Street, Los Angeles, CA 90033, USA.

Abstract

Asthma is the result of chronic airway inflammation associated predominantly with CD4+ cells, eosinophils, mast cells, and basophils. Several T-cells subsets, including NKT cells, play a critical role in orchestrating the inflammation in the airways predominantly, by secreting interleukin-4 and interleukin-13. Recently, programmed death-1 (PD-1) with its ligands, programmed death ligand B7H1 (PD-L1) and B7DC (PD-L2), was shown to regulate T-cell activation and tolerance. PD-1 has been characterized as a negative regulator of conventional CD4+T cells. In addition, the relative roles of PD-L1 and PD-L2 in regulating the activation and function of T cells have recently been characterized. Recent studies have demonstrated that PD-L1 and PD-L2 have important but opposing roles in modulating and polarizing T-cell functions in airway hyperreactivity. Whereas the severity of asthma is greatly enhanced in absence of PD-L2, PD-L1 deficiency resulted in reduced airway hyperresponsiveness and only minimal inflammation. This observation is partially because of the polarization of NKT cells in PD-L1- and PD-L2-deficient mice. This review will discuss the recent literature regarding the role of PD-L1 and PD-L2 in allergic disease and asthma. Current understanding of the role of PD ligands in allergic asthma gives impetus to the development of novel therapeutic approaches.

© 2010 John Wiley & Sons A/S.

PMID:
20722638
[PubMed - indexed for MEDLINE]
PMCID:
PMC3017219
Free PMC Article

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