Age-related increases in PGD(2) expression impair respiratory DC migration, resulting in diminished T cell responses upon respiratory virus infection in mice.
Identifieur interne : 002155 ( Main/Exploration ); précédent : 002154; suivant : 002156Age-related increases in PGD(2) expression impair respiratory DC migration, resulting in diminished T cell responses upon respiratory virus infection in mice.
Auteurs : Jincun Zhao [États-Unis] ; Jingxian Zhao ; Kevin Legge ; Stanley PerlmanSource :
- The Journal of clinical investigation [ 1558-8238 ] ; 2011.
Descripteurs français
- KwdFr :
- Activation des lymphocytes, Animaux, Antagonistes des prostaglandines (pharmacologie), Antagonistes des prostaglandines (usage thérapeutique), Cellules dendritiques (anatomopathologie), Cellules dendritiques (immunologie), Infections à Orthomyxoviridae (immunologie), Infections à Orthomyxoviridae (métabolisme), Infections à Orthomyxoviridae (virologie), Infections à coronavirus (immunologie), Infections à coronavirus (métabolisme), Infections à coronavirus (virologie), Infections à virus respiratoire syncytial (immunologie), Infections à virus respiratoire syncytial (métabolisme), Infections à virus respiratoire syncytial (virologie), Microenvironnement cellulaire (immunologie), Mouvement cellulaire (), Noeuds lymphatiques (anatomopathologie), Noeuds lymphatiques (immunologie), Organismes exempts d'organismes pathogènes spécifiques, Poumon (anatomopathologie), Poumon (immunologie), Prostaglandine D2 (biosynthèse), Prostaglandine D2 (physiologie), Récepteurs CCR7 (biosynthèse), Récepteurs CCR7 (génétique), Souris, Souris de lignée C57BL, Sous-populations de lymphocytes T (immunologie), Sujet immunodéprimé, Susceptibilité à une maladie, Syndrome respiratoire aigu sévère (immunologie), Syndrome respiratoire aigu sévère (métabolisme), Syndrome respiratoire aigu sévère (virologie), Vieillissement (métabolisme), Virus de l'hépatite murine (immunologie), Virus de la grippe A (immunologie), Virus du SRAS (immunologie), Virus respiratoires syncytiaux (immunologie).
- MESH :
- anatomopathologie : Cellules dendritiques, Noeuds lymphatiques, Poumon.
- biosynthèse : Prostaglandine D2, Récepteurs CCR7.
- génétique : Récepteurs CCR7.
- immunologie : Cellules dendritiques, Infections à Orthomyxoviridae, Infections à coronavirus, Infections à virus respiratoire syncytial, Microenvironnement cellulaire, Noeuds lymphatiques, Poumon, Sous-populations de lymphocytes T, Syndrome respiratoire aigu sévère, Virus de l'hépatite murine, Virus de la grippe A, Virus du SRAS, Virus respiratoires syncytiaux.
- métabolisme : Infections à Orthomyxoviridae, Infections à coronavirus, Infections à virus respiratoire syncytial, Syndrome respiratoire aigu sévère, Vieillissement.
- pharmacologie : Antagonistes des prostaglandines.
- physiologie : Prostaglandine D2.
- usage thérapeutique : Antagonistes des prostaglandines.
- virologie : Infections à Orthomyxoviridae, Infections à coronavirus, Infections à virus respiratoire syncytial, Syndrome respiratoire aigu sévère.
- Activation des lymphocytes, Animaux, Mouvement cellulaire, Organismes exempts d'organismes pathogènes spécifiques, Souris, Souris de lignée C57BL, Sujet immunodéprimé, Susceptibilité à une maladie.
English descriptors
- KwdEn :
- Aging (metabolism), Animals, Cell Movement (drug effects), Cellular Microenvironment (immunology), Coronavirus Infections (immunology), Coronavirus Infections (metabolism), Coronavirus Infections (virology), Dendritic Cells (immunology), Dendritic Cells (pathology), Disease Susceptibility, Immunocompromised Host, Influenza A virus (immunology), Lung (immunology), Lung (pathology), Lymph Nodes (immunology), Lymph Nodes (pathology), Lymphocyte Activation, Mice, Mice, Inbred C57BL, Murine hepatitis virus (immunology), Orthomyxoviridae Infections (immunology), Orthomyxoviridae Infections (metabolism), Orthomyxoviridae Infections (virology), Prostaglandin Antagonists (pharmacology), Prostaglandin Antagonists (therapeutic use), Prostaglandin D2 (biosynthesis), Prostaglandin D2 (physiology), Receptors, CCR7 (biosynthesis), Receptors, CCR7 (genetics), Respiratory Syncytial Virus Infections (immunology), Respiratory Syncytial Virus Infections (metabolism), Respiratory Syncytial Virus Infections (virology), Respiratory Syncytial Viruses (immunology), SARS Virus (immunology), Severe Acute Respiratory Syndrome (immunology), Severe Acute Respiratory Syndrome (metabolism), Severe Acute Respiratory Syndrome (virology), Specific Pathogen-Free Organisms, T-Lymphocyte Subsets (immunology).
- MESH :
- chemical , biosynthesis : Prostaglandin D2, Receptors, CCR7.
- chemical , genetics : Receptors, CCR7.
- chemical , pharmacology : Prostaglandin Antagonists.
- drug effects : Cell Movement.
- immunology : Cellular Microenvironment, Coronavirus Infections, Dendritic Cells, Influenza A virus, Lung, Lymph Nodes, Murine hepatitis virus, Orthomyxoviridae Infections, Respiratory Syncytial Virus Infections, Respiratory Syncytial Viruses, SARS Virus, Severe Acute Respiratory Syndrome, T-Lymphocyte Subsets.
- metabolism : Aging, Coronavirus Infections, Orthomyxoviridae Infections, Respiratory Syncytial Virus Infections, Severe Acute Respiratory Syndrome.
- pathology : Dendritic Cells, Lung, Lymph Nodes.
- chemical , physiology : Prostaglandin D2.
- chemical , therapeutic use : Prostaglandin Antagonists.
- virology : Coronavirus Infections, Orthomyxoviridae Infections, Respiratory Syncytial Virus Infections, Severe Acute Respiratory Syndrome.
- Animals, Disease Susceptibility, Immunocompromised Host, Lymphocyte Activation, Mice, Mice, Inbred C57BL, Specific Pathogen-Free Organisms.
Abstract
The morbidity and mortality associated with respiratory virus infection is felt most keenly among the elderly. T cells are necessary for viral clearance, and many age-dependent intrinsic T cell defects have been documented. However, the development of robust T cell responses in the lung also requires respiratory DCs (rDCs), which must process antigen and migrate to draining LNs (DLNs), and little is known about age-related defects in these T cell-extrinsic functions. Here, we show that increases in prostaglandin D(2) (PGD(2)) expression in mouse lungs upon aging correlate with a progressive impairment in rDC migration to DLNs. Decreased rDC migration resulted in diminished T cell responses and more severe clinical disease in older mice infected with respiratory viruses. Diminished rDC migration associated with virus-specific defects in T cell responses and was not a result of cell-intrinsic defect, rather it reflected the observed age-dependent increases in PGD(2) expression. Blocking PGD(2) function with small-molecule antagonists enhanced rDC migration, T cell responses, and survival. This effect correlated with upregulation on rDCs of CCR7, a chemokine receptor involved in DC chemotaxis. Our results suggest that inhibiting PGD(2) function may be a useful approach to enhance T cell responses against respiratory viruses in older humans.
DOI: 10.1172/JCI59777
PubMed: 22105170
Affiliations:
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Le document en format XML
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<profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Aging (metabolism)</term>
<term>Animals</term>
<term>Cell Movement (drug effects)</term>
<term>Cellular Microenvironment (immunology)</term>
<term>Coronavirus Infections (immunology)</term>
<term>Coronavirus Infections (metabolism)</term>
<term>Coronavirus Infections (virology)</term>
<term>Dendritic Cells (immunology)</term>
<term>Dendritic Cells (pathology)</term>
<term>Disease Susceptibility</term>
<term>Immunocompromised Host</term>
<term>Influenza A virus (immunology)</term>
<term>Lung (immunology)</term>
<term>Lung (pathology)</term>
<term>Lymph Nodes (immunology)</term>
<term>Lymph Nodes (pathology)</term>
<term>Lymphocyte Activation</term>
<term>Mice</term>
<term>Mice, Inbred C57BL</term>
<term>Murine hepatitis virus (immunology)</term>
<term>Orthomyxoviridae Infections (immunology)</term>
<term>Orthomyxoviridae Infections (metabolism)</term>
<term>Orthomyxoviridae Infections (virology)</term>
<term>Prostaglandin Antagonists (pharmacology)</term>
<term>Prostaglandin Antagonists (therapeutic use)</term>
<term>Prostaglandin D2 (biosynthesis)</term>
<term>Prostaglandin D2 (physiology)</term>
<term>Receptors, CCR7 (biosynthesis)</term>
<term>Receptors, CCR7 (genetics)</term>
<term>Respiratory Syncytial Virus Infections (immunology)</term>
<term>Respiratory Syncytial Virus Infections (metabolism)</term>
<term>Respiratory Syncytial Virus Infections (virology)</term>
<term>Respiratory Syncytial Viruses (immunology)</term>
<term>SARS Virus (immunology)</term>
<term>Severe Acute Respiratory Syndrome (immunology)</term>
<term>Severe Acute Respiratory Syndrome (metabolism)</term>
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<term>T-Lymphocyte Subsets (immunology)</term>
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<term>Animaux</term>
<term>Antagonistes des prostaglandines (pharmacologie)</term>
<term>Antagonistes des prostaglandines (usage thérapeutique)</term>
<term>Cellules dendritiques (anatomopathologie)</term>
<term>Cellules dendritiques (immunologie)</term>
<term>Infections à Orthomyxoviridae (immunologie)</term>
<term>Infections à Orthomyxoviridae (métabolisme)</term>
<term>Infections à Orthomyxoviridae (virologie)</term>
<term>Infections à coronavirus (immunologie)</term>
<term>Infections à coronavirus (métabolisme)</term>
<term>Infections à coronavirus (virologie)</term>
<term>Infections à virus respiratoire syncytial (immunologie)</term>
<term>Infections à virus respiratoire syncytial (métabolisme)</term>
<term>Infections à virus respiratoire syncytial (virologie)</term>
<term>Microenvironnement cellulaire (immunologie)</term>
<term>Mouvement cellulaire ()</term>
<term>Noeuds lymphatiques (anatomopathologie)</term>
<term>Noeuds lymphatiques (immunologie)</term>
<term>Organismes exempts d'organismes pathogènes spécifiques</term>
<term>Poumon (anatomopathologie)</term>
<term>Poumon (immunologie)</term>
<term>Prostaglandine D2 (biosynthèse)</term>
<term>Prostaglandine D2 (physiologie)</term>
<term>Récepteurs CCR7 (biosynthèse)</term>
<term>Récepteurs CCR7 (génétique)</term>
<term>Souris</term>
<term>Souris de lignée C57BL</term>
<term>Sous-populations de lymphocytes T (immunologie)</term>
<term>Sujet immunodéprimé</term>
<term>Susceptibilité à une maladie</term>
<term>Syndrome respiratoire aigu sévère (immunologie)</term>
<term>Syndrome respiratoire aigu sévère (métabolisme)</term>
<term>Syndrome respiratoire aigu sévère (virologie)</term>
<term>Vieillissement (métabolisme)</term>
<term>Virus de l'hépatite murine (immunologie)</term>
<term>Virus de la grippe A (immunologie)</term>
<term>Virus du SRAS (immunologie)</term>
<term>Virus respiratoires syncytiaux (immunologie)</term>
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<keywords scheme="MESH" type="chemical" qualifier="biosynthesis" xml:lang="en"><term>Prostaglandin D2</term>
<term>Receptors, CCR7</term>
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<keywords scheme="MESH" type="chemical" qualifier="genetics" xml:lang="en"><term>Receptors, CCR7</term>
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<keywords scheme="MESH" type="chemical" qualifier="pharmacology" xml:lang="en"><term>Prostaglandin Antagonists</term>
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<keywords scheme="MESH" qualifier="anatomopathologie" xml:lang="fr"><term>Cellules dendritiques</term>
<term>Noeuds lymphatiques</term>
<term>Poumon</term>
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<keywords scheme="MESH" qualifier="biosynthèse" xml:lang="fr"><term>Prostaglandine D2</term>
<term>Récepteurs CCR7</term>
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<keywords scheme="MESH" qualifier="drug effects" xml:lang="en"><term>Cell Movement</term>
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<keywords scheme="MESH" qualifier="génétique" xml:lang="fr"><term>Récepteurs CCR7</term>
</keywords>
<keywords scheme="MESH" qualifier="immunologie" xml:lang="fr"><term>Cellules dendritiques</term>
<term>Infections à Orthomyxoviridae</term>
<term>Infections à coronavirus</term>
<term>Infections à virus respiratoire syncytial</term>
<term>Microenvironnement cellulaire</term>
<term>Noeuds lymphatiques</term>
<term>Poumon</term>
<term>Sous-populations de lymphocytes T</term>
<term>Syndrome respiratoire aigu sévère</term>
<term>Virus de l'hépatite murine</term>
<term>Virus de la grippe A</term>
<term>Virus du SRAS</term>
<term>Virus respiratoires syncytiaux</term>
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<term>Coronavirus Infections</term>
<term>Dendritic Cells</term>
<term>Influenza A virus</term>
<term>Lung</term>
<term>Lymph Nodes</term>
<term>Murine hepatitis virus</term>
<term>Orthomyxoviridae Infections</term>
<term>Respiratory Syncytial Virus Infections</term>
<term>Respiratory Syncytial Viruses</term>
<term>SARS Virus</term>
<term>Severe Acute Respiratory Syndrome</term>
<term>T-Lymphocyte Subsets</term>
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<term>Coronavirus Infections</term>
<term>Orthomyxoviridae Infections</term>
<term>Respiratory Syncytial Virus Infections</term>
<term>Severe Acute Respiratory Syndrome</term>
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<term>Infections à coronavirus</term>
<term>Infections à virus respiratoire syncytial</term>
<term>Syndrome respiratoire aigu sévère</term>
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<term>Lung</term>
<term>Lymph Nodes</term>
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<keywords scheme="MESH" qualifier="pharmacologie" xml:lang="fr"><term>Antagonistes des prostaglandines</term>
</keywords>
<keywords scheme="MESH" qualifier="physiologie" xml:lang="fr"><term>Prostaglandine D2</term>
</keywords>
<keywords scheme="MESH" type="chemical" qualifier="physiology" xml:lang="en"><term>Prostaglandin D2</term>
</keywords>
<keywords scheme="MESH" type="chemical" qualifier="therapeutic use" xml:lang="en"><term>Prostaglandin Antagonists</term>
</keywords>
<keywords scheme="MESH" qualifier="usage thérapeutique" xml:lang="fr"><term>Antagonistes des prostaglandines</term>
</keywords>
<keywords scheme="MESH" qualifier="virologie" xml:lang="fr"><term>Infections à Orthomyxoviridae</term>
<term>Infections à coronavirus</term>
<term>Infections à virus respiratoire syncytial</term>
<term>Syndrome respiratoire aigu sévère</term>
</keywords>
<keywords scheme="MESH" qualifier="virology" xml:lang="en"><term>Coronavirus Infections</term>
<term>Orthomyxoviridae Infections</term>
<term>Respiratory Syncytial Virus Infections</term>
<term>Severe Acute Respiratory Syndrome</term>
</keywords>
<keywords scheme="MESH" xml:lang="en"><term>Animals</term>
<term>Disease Susceptibility</term>
<term>Immunocompromised Host</term>
<term>Lymphocyte Activation</term>
<term>Mice</term>
<term>Mice, Inbred C57BL</term>
<term>Specific Pathogen-Free Organisms</term>
</keywords>
<keywords scheme="MESH" xml:lang="fr"><term>Activation des lymphocytes</term>
<term>Animaux</term>
<term>Mouvement cellulaire</term>
<term>Organismes exempts d'organismes pathogènes spécifiques</term>
<term>Souris</term>
<term>Souris de lignée C57BL</term>
<term>Sujet immunodéprimé</term>
<term>Susceptibilité à une maladie</term>
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<front><div type="abstract" xml:lang="en">The morbidity and mortality associated with respiratory virus infection is felt most keenly among the elderly. T cells are necessary for viral clearance, and many age-dependent intrinsic T cell defects have been documented. However, the development of robust T cell responses in the lung also requires respiratory DCs (rDCs), which must process antigen and migrate to draining LNs (DLNs), and little is known about age-related defects in these T cell-extrinsic functions. Here, we show that increases in prostaglandin D(2) (PGD(2)) expression in mouse lungs upon aging correlate with a progressive impairment in rDC migration to DLNs. Decreased rDC migration resulted in diminished T cell responses and more severe clinical disease in older mice infected with respiratory viruses. Diminished rDC migration associated with virus-specific defects in T cell responses and was not a result of cell-intrinsic defect, rather it reflected the observed age-dependent increases in PGD(2) expression. Blocking PGD(2) function with small-molecule antagonists enhanced rDC migration, T cell responses, and survival. This effect correlated with upregulation on rDCs of CCR7, a chemokine receptor involved in DC chemotaxis. Our results suggest that inhibiting PGD(2) function may be a useful approach to enhance T cell responses against respiratory viruses in older humans.</div>
</front>
</TEI>
<affiliations><list><country><li>États-Unis</li>
</country>
<region><li>Iowa</li>
</region>
<settlement><li>Iowa City</li>
</settlement>
<orgName><li>Université de l'Iowa</li>
</orgName>
</list>
<tree><noCountry><name sortKey="Legge, Kevin" sort="Legge, Kevin" uniqKey="Legge K" first="Kevin" last="Legge">Kevin Legge</name>
<name sortKey="Perlman, Stanley" sort="Perlman, Stanley" uniqKey="Perlman S" first="Stanley" last="Perlman">Stanley Perlman</name>
<name sortKey="Zhao, Jingxian" sort="Zhao, Jingxian" uniqKey="Zhao J" first="Jingxian" last="Zhao">Jingxian Zhao</name>
</noCountry>
<country name="États-Unis"><region name="Iowa"><name sortKey="Zhao, Jincun" sort="Zhao, Jincun" uniqKey="Zhao J" first="Jincun" last="Zhao">Jincun Zhao</name>
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