CD200 Receptor Controls Sex-Specific TLR7 Responses to Viral Infection
Identifieur interne : 000B84 ( Main/Curation ); précédent : 000B83; suivant : 000B85CD200 Receptor Controls Sex-Specific TLR7 Responses to Viral Infection
Auteurs : Guruswamy Karnam [Pays-Bas] ; Tomasz P. Rygiel [Pays-Bas] ; Matthijs Raaben [Pays-Bas] ; Guy C. M. Grinwis [Pays-Bas] ; Frank E. Coenjaerts [Pays-Bas] ; Maaike E. Ressing [Pays-Bas] ; Peter J. M. Rottier [Pays-Bas] ; Cornelis A. M. De Haan [Pays-Bas] ; Linde Meyaard [Pays-Bas]Source :
- PLoS Pathogens [ 1553-7366 ] ; 2012.
Descripteurs français
- KwdFr :
- Animaux, Antigènes CD (génétique), Antigènes CD (métabolisme), Caractères sexuels, Femelle, Glycoprotéines membranaires (immunologie), Glycoprotéines membranaires (métabolisme), Granulocytes neutrophiles (immunologie), Granulocytes neutrophiles (métabolisme), Infections à Orthomyxoviridae (immunologie), Infections à coronavirus (immunologie), Infiltration par les neutrophiles, Interféron de type I (biosynthèse), Récepteur de type Toll-7 (immunologie), Récepteur de type Toll-7 (métabolisme), Souris, Souris de lignée C57BL, Souris knockout, Transduction du signal, Virus de l'hépatite murine, Virus de la grippe A (immunologie), Virus de la grippe A (pathogénicité).
- MESH :
- biosynthèse : Interféron de type I.
- génétique : Antigènes CD.
- immunologie : Glycoprotéines membranaires, Granulocytes neutrophiles, Infections à Orthomyxoviridae, Infections à coronavirus, Récepteur de type Toll-7, Virus de la grippe A.
- métabolisme : Antigènes CD, Glycoprotéines membranaires, Granulocytes neutrophiles, Récepteur de type Toll-7.
- pathogénicité : Virus de la grippe A.
- Animaux, Caractères sexuels, Femelle, Infiltration par les neutrophiles, Souris, Souris de lignée C57BL, Souris knockout, Transduction du signal, Virus de l'hépatite murine.
English descriptors
- KwdEn :
- Animals, Antigens, CD (genetics), Antigens, CD (metabolism), Coronavirus Infections (immunology), Female, Influenza A virus (immunology), Influenza A virus (pathogenicity), Interferon Type I (biosynthesis), Membrane Glycoproteins (immunology), Membrane Glycoproteins (metabolism), Mice, Mice, Inbred C57BL, Mice, Knockout, Murine hepatitis virus, Neutrophil Infiltration, Neutrophils (immunology), Neutrophils (metabolism), Orthomyxoviridae Infections (immunology), Sex Characteristics, Signal Transduction, Toll-Like Receptor 7 (immunology), Toll-Like Receptor 7 (metabolism).
- MESH :
- chemical , biosynthesis : Interferon Type I.
- chemical , genetics : Antigens, CD.
- chemical , immunology : Membrane Glycoproteins, Toll-Like Receptor 7.
- chemical , metabolism : Antigens, CD, Membrane Glycoproteins, Toll-Like Receptor 7.
- immunology : Coronavirus Infections, Influenza A virus, Neutrophils, Orthomyxoviridae Infections.
- metabolism : Neutrophils.
- pathogenicity : Influenza A virus.
- Animals, Female, Mice, Mice, Inbred C57BL, Mice, Knockout, Murine hepatitis virus, Neutrophil Infiltration, Sex Characteristics, Signal Transduction.
Abstract
Immunological checkpoints, such as the inhibitory CD200 receptor (CD200R), play a dual role in balancing the immune system during microbial infection. On the one hand these inhibitory signals prevent excessive immune mediated pathology but on the other hand they may impair clearance of the pathogen. We studied the influence of the inhibitory CD200-CD200R axis on clearance and pathology in two different virus infection models. We find that lack of CD200R signaling strongly enhances type I interferon (IFN) production and viral clearance and improves the outcome of mouse hepatitis corona virus (MHV) infection, particularly in female mice. MHV clearance is known to be dependent on Toll like receptor 7 (TLR7)-mediated type I IFN production and sex differences in TLR7 responses previously have been reported for humans. We therefore hypothesize that CD200R ligation suppresses TLR7 responses and that release of this inhibition enlarges sex differences in TLR7 signaling. This hypothesis is supported by our findings that
Url:
DOI: 10.1371/journal.ppat.1002710
PubMed: 22615569
PubMed Central: 3355091
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PMC:3355091Le document en format XML
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<profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Animals</term>
<term>Antigens, CD (genetics)</term>
<term>Antigens, CD (metabolism)</term>
<term>Coronavirus Infections (immunology)</term>
<term>Female</term>
<term>Influenza A virus (immunology)</term>
<term>Influenza A virus (pathogenicity)</term>
<term>Interferon Type I (biosynthesis)</term>
<term>Membrane Glycoproteins (immunology)</term>
<term>Membrane Glycoproteins (metabolism)</term>
<term>Mice</term>
<term>Mice, Inbred C57BL</term>
<term>Mice, Knockout</term>
<term>Murine hepatitis virus</term>
<term>Neutrophil Infiltration</term>
<term>Neutrophils (immunology)</term>
<term>Neutrophils (metabolism)</term>
<term>Orthomyxoviridae Infections (immunology)</term>
<term>Sex Characteristics</term>
<term>Signal Transduction</term>
<term>Toll-Like Receptor 7 (immunology)</term>
<term>Toll-Like Receptor 7 (metabolism)</term>
</keywords>
<keywords scheme="KwdFr" xml:lang="fr"><term>Animaux</term>
<term>Antigènes CD (génétique)</term>
<term>Antigènes CD (métabolisme)</term>
<term>Caractères sexuels</term>
<term>Femelle</term>
<term>Glycoprotéines membranaires (immunologie)</term>
<term>Glycoprotéines membranaires (métabolisme)</term>
<term>Granulocytes neutrophiles (immunologie)</term>
<term>Granulocytes neutrophiles (métabolisme)</term>
<term>Infections à Orthomyxoviridae (immunologie)</term>
<term>Infections à coronavirus (immunologie)</term>
<term>Infiltration par les neutrophiles</term>
<term>Interféron de type I (biosynthèse)</term>
<term>Récepteur de type Toll-7 (immunologie)</term>
<term>Récepteur de type Toll-7 (métabolisme)</term>
<term>Souris</term>
<term>Souris de lignée C57BL</term>
<term>Souris knockout</term>
<term>Transduction du signal</term>
<term>Virus de l'hépatite murine</term>
<term>Virus de la grippe A (immunologie)</term>
<term>Virus de la grippe A (pathogénicité)</term>
</keywords>
<keywords scheme="MESH" type="chemical" qualifier="biosynthesis" xml:lang="en"><term>Interferon Type I</term>
</keywords>
<keywords scheme="MESH" type="chemical" qualifier="genetics" xml:lang="en"><term>Antigens, CD</term>
</keywords>
<keywords scheme="MESH" type="chemical" qualifier="immunology" xml:lang="en"><term>Membrane Glycoproteins</term>
<term>Toll-Like Receptor 7</term>
</keywords>
<keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>Antigens, CD</term>
<term>Membrane Glycoproteins</term>
<term>Toll-Like Receptor 7</term>
</keywords>
<keywords scheme="MESH" qualifier="biosynthèse" xml:lang="fr"><term>Interféron de type I</term>
</keywords>
<keywords scheme="MESH" qualifier="génétique" xml:lang="fr"><term>Antigènes CD</term>
</keywords>
<keywords scheme="MESH" qualifier="immunologie" xml:lang="fr"><term>Glycoprotéines membranaires</term>
<term>Granulocytes neutrophiles</term>
<term>Infections à Orthomyxoviridae</term>
<term>Infections à coronavirus</term>
<term>Récepteur de type Toll-7</term>
<term>Virus de la grippe A</term>
</keywords>
<keywords scheme="MESH" qualifier="immunology" xml:lang="en"><term>Coronavirus Infections</term>
<term>Influenza A virus</term>
<term>Neutrophils</term>
<term>Orthomyxoviridae Infections</term>
</keywords>
<keywords scheme="MESH" qualifier="metabolism" xml:lang="en"><term>Neutrophils</term>
</keywords>
<keywords scheme="MESH" qualifier="métabolisme" xml:lang="fr"><term>Antigènes CD</term>
<term>Glycoprotéines membranaires</term>
<term>Granulocytes neutrophiles</term>
<term>Récepteur de type Toll-7</term>
</keywords>
<keywords scheme="MESH" qualifier="pathogenicity" xml:lang="en"><term>Influenza A virus</term>
</keywords>
<keywords scheme="MESH" qualifier="pathogénicité" xml:lang="fr"><term>Virus de la grippe A</term>
</keywords>
<keywords scheme="MESH" xml:lang="en"><term>Animals</term>
<term>Female</term>
<term>Mice</term>
<term>Mice, Inbred C57BL</term>
<term>Mice, Knockout</term>
<term>Murine hepatitis virus</term>
<term>Neutrophil Infiltration</term>
<term>Sex Characteristics</term>
<term>Signal Transduction</term>
</keywords>
<keywords scheme="MESH" xml:lang="fr"><term>Animaux</term>
<term>Caractères sexuels</term>
<term>Femelle</term>
<term>Infiltration par les neutrophiles</term>
<term>Souris</term>
<term>Souris de lignée C57BL</term>
<term>Souris knockout</term>
<term>Transduction du signal</term>
<term>Virus de l'hépatite murine</term>
</keywords>
</textClass>
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</teiHeader>
<front><div type="abstract" xml:lang="en"><p>Immunological checkpoints, such as the inhibitory CD200 receptor (CD200R), play a dual role in balancing the immune system during microbial infection. On the one hand these inhibitory signals prevent excessive immune mediated pathology but on the other hand they may impair clearance of the pathogen. We studied the influence of the inhibitory CD200-CD200R axis on clearance and pathology in two different virus infection models. We find that lack of CD200R signaling strongly enhances type I interferon (IFN) production and viral clearance and improves the outcome of mouse hepatitis corona virus (MHV) infection, particularly in female mice. MHV clearance is known to be dependent on Toll like receptor 7 (TLR7)-mediated type I IFN production and sex differences in TLR7 responses previously have been reported for humans. We therefore hypothesize that CD200R ligation suppresses TLR7 responses and that release of this inhibition enlarges sex differences in TLR7 signaling. This hypothesis is supported by our findings that <italic>in vivo</italic>
administration of synthetic TLR7 ligand leads to enhanced type I IFN production, particularly in female <italic>Cd200<sup>−/−</sup>
</italic>
mice and that CD200R ligation inhibits TLR7 signaling <italic>in vitro</italic>
. In influenza A virus infection we show that viral clearance is determined by sex but not by CD200R signaling. However, absence of CD200R in influenza A virus infection results in enhanced lung neutrophil influx and pathology in females. Thus, CD200-CD200R and sex are host factors that together determine the outcome of viral infection. Our data predict a sex bias in both beneficial and pathological immune responses to virus infection upon therapeutic targeting of CD200-CD200R.</p>
</div>
</front>
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</TEI>
</record>
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