NDLI: OX40 ligand and programmed cell death 1 ligand 2 expression on inflammatory dendritic cells regulates CD4 T cell cytokine production in the lung during viral disease.

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OX40 ligand and programmed cell death 1 ligand 2 expression on inflammatory dendritic cells regulates CD4 T cell cytokine production in the lung during viral disease.

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OX40 ligand and programmed cell death 1 ligand 2 expression on inflammatory dendritic cells regulates CD4 T cell cytokine production in the lung during viral disease.

Content Provider	World Health Organization (WHO)-Global Index Medicus
Author	Dodd, Jonathan S. Openshaw, Peter J. Schwarze, Jürgen Wythe, Sarah E.
Description	Country affiliation: United kingdom Author Affiliation: Wythe SE ( Center for Respiratory Infections, National Heart and Lung Institute, St. Mary's Campus, Imperial College London, London W2 1PG, UK.)
Abstract	CD4 Th differentiation is influenced by costimulatory molecules expressed on conventional dendritic cells (DCs) in regional lymph nodes and results in specific patterns of cytokine production. However, the function of costimulatory molecules on inflammatory (CD11b(+)) DCs in the lung during recall responses is not fully understood, but it is important for development of novel interventions to limit immunopathological responses to infection. Using a mouse model in which vaccination with vaccinia virus vectors expressing the respiratory syncytial virus (RSV) fusion protein (rVVF) or attachment protein (rVVG) leads to type 1- or type 2-biased cytokine responses, respectively, upon RSV challenge, we found expression of CD40 and OX40 ligand (OX40L) on lung inflammatory DCs was higher in rVVF-primed mice than in rVVG-primed mice early after RSV challenge, whereas the reverse was observed later in the response. Conversely, programmed cell death 1 ligand 2 (PD-L2) was higher in rVVG-primed mice throughout. Inflammatory DCs isolated at the resolution of inflammation revealed that OX40L on type 1-biased DCs promoted IL-5, whereas OX40L on type 2-biased DCs enhanced IFN-Î³ production by Ag-reactive Th cells. In contrast, PD-L2 promoted IFN-Î³ production, irrespective of conditions, suppressing IL-5 only if expressed on type 1-biased DCs. Thus, OX40L and PD-L2 expressed on DCs differentially regulate cytokine production during recall responses in the lung. Manipulation of these costimulatory pathways may provide a novel approach to controlling pulmonary inflammatory responses.
ISSN	00221767
e-ISSN	15506606
DOI	10.4049/jimmunol.1103001
Journal	The Journal of Immunology
Issue Number	4
Volume Number	188
Language	English
Publisher	The American Association of Immunologists
Publisher Date	2012-02-15
Publisher Place	United States
Access Restriction	Open
Subject Keyword	Cd4-positive T-lymphocytes Immunology Cytokines Biosynthesis Dendritic Cells Lung Membrane Glycoproteins Programmed Cell Death 1 Ligand 2 Protein Respiratory Syncytial Virus Infections Tumor Necrosis Factors Animals Metabolism Immunologic Memory Interferon-gamma Interleukin-5 Pathology Mice Mice, Inbred Balb C Respiratory Syncytial Virus Vaccines Respiratory Syncytial Viruses Genetics Vaccinia Virus Viral Fusion Proteins Research Support, Non-u.s. Gov't Discipline Immunology
Content Type	Text
Resource Type	Article
Subject	Immunology and Allergy Immunology

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