RGD Reference Report - Cytomegalovirus-Specific IL-10-Producing CD4+ T Cells Are Governed by Type-I IFN-Induced IL-27 and Promote Virus Persistence. - Rat Genome Database

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Cytomegalovirus-Specific IL-10-Producing CD4+ T Cells Are Governed by Type-I IFN-Induced IL-27 and Promote Virus Persistence.

Authors: Clement, Mathew  Marsden, Morgan  Stacey, Maria A  Abdul-Karim, Juneid  Gimeno Brias, Silvia  Costa Bento, Diana  Scurr, Martin J  Ghazal, Peter  Weaver, Casey T  Carlesso, Gianluca  Clare, Simon  Jones, Simon A  Godkin, Andrew  Jones, Gareth W  Humphreys, Ian R 
Citation: Clement M, etal., PLoS Pathog. 2016 Dec 7;12(12):e1006050. doi: 10.1371/journal.ppat.1006050. eCollection 2016 Dec.
RGD ID: 126790498
Pubmed: PMID:27926930   (View Abstract at PubMed)
PMCID: PMC5142785   (View Article at PubMed Central)
DOI: DOI:10.1371/journal.ppat.1006050   (Journal Full-text)

CD4+ T cells support host defence against herpesviruses and other viral pathogens. We identified that CD4+ T cells from systemic and mucosal tissues of hosts infected with the β-herpesviridae human cytomegalovirus (HCMV) or murine cytomegalovirus (MCMV) express the regulatory cytokine interleukin (IL)-10. IL-10+CD4+ T cells co-expressed TH1-associated transcription factors and chemokine receptors. Mice lacking T cell-derived IL-10 elicited enhanced antiviral T cell responses and restricted MCMV persistence in salivary glands and secretion in saliva. Thus, IL-10+CD4+ T cells suppress antiviral immune responses against CMV. Expansion of this T-cell population in the periphery was promoted by IL-27 whereas mucosal IL-10+ T cell responses were ICOS-dependent. Infected Il27rα-deficient mice with reduced peripheral IL-10+CD4+ T cell accumulation displayed robust T cell responses and restricted MCMV persistence and shedding. Temporal inhibition experiments revealed that IL-27R signaling during initial infection was required for the suppression of T cell immunity and control of virus shedding during MCMV persistence. IL-27 production was promoted by type-I IFN, suggesting that β-herpesviridae exploit the immune-regulatory properties of this antiviral pathway to establish chronicity. Further, our data reveal that cytokine signaling events during initial infection profoundly influence virus chronicity.



RGD Manual Disease Annotations    Click to see Annotation Detail View

  
Object SymbolSpeciesTermQualifierEvidenceWithNotesSourceOriginal Reference(s)
IL27HumanCytomegalovirus Infections  ISOIl27 (Mus musculus)protein:increased expression:spleen and saliva-secreting gland (mouse)RGD 
Il27RatCytomegalovirus Infections  ISOIl27 (Mus musculus)protein:increased expression:spleen and saliva-secreting gland (mouse)RGD 
Il27MouseCytomegalovirus Infections  IEP protein:increased expression:spleen and saliva-secreting gland (mouse)RGD 

Objects Annotated

Genes (Rattus norvegicus)
Il27  (interleukin 27)

Genes (Mus musculus)
Il27  (interleukin 27)

Genes (Homo sapiens)
IL27  (interleukin 27)


Additional Information