The role of Th17 and Treg responses in the pathogenesis of RSV infection.
The respiratory syncytial virus (RSV) represents the leading cause of viral bronchiolitis and pneumonia in children worldwide and is associated with high morbidity, hospitalization rate, and significant mortality rates. The immune response elicited by RSV is one of the main factors contributing to the pathogenesis of the disease. Two subsets of the cellular immune response, the T helper 17 cell (Th17) and the regulatory T-cell (Treg), and more particularly the balance between these two subsets, might play a significant role in the pathogenesis of the RSV infection. The developmental pathways of Th17 and Treg cells are closely and reciprocally interconnected and plasticity has been demonstrated from Treg toward Th17. During an RSV infection, the functions of both subsets are opposed to one another regarding viral clearance and clinical severity. Th17 and Treg cells offer a promising new view on the pathogenesis of an RSV infection and deserve further exploration.
Faculty of Medicine and Health Sciences, University of Antwerp, Antwerp, Belgium.
Thomas C
TC
Mangodt
Faculty of Medicine and Health Sciences, University of Antwerp, Antwerp, Belgium.
Mikhaïl A
MA
Van Herck
Laboratory of Experimental Medicine and Pediatrics, University of Antwerp, Antwerp, Belgium.
Sara
S
Nullens
Faculty of Medicine and Health Sciences, University of Antwerp, Antwerp, Belgium.|Laboratory of Experimental Medicine and Pediatrics, University of Antwerp, Antwerp, Belgium.|Department of Pediatrics, Antwerp University Hospital, Edegem, Belgium.
José
J
Ramet
Laboratory of Experimental Medicine and Pediatrics, University of Antwerp, Antwerp, Belgium.|Department of Critical Care Medicine, Antwerp University Hospital, Edegem, Belgium.
Jozef J
JJ
De Dooy
Faculty of Medicine and Health Sciences, University of Antwerp, Antwerp, Belgium.|Laboratory of Experimental Medicine and Pediatrics, University of Antwerp, Antwerp, Belgium.|Department of Critical Care Medicine, Antwerp University Hospital, Edegem, Belgium.
Philippe G
PG
Jorens
Laboratory of Experimental Medicine and Pediatrics, University of Antwerp, Antwerp, Belgium.
Benedicte Y
BY
De Winter
D000818:Animals; D002450:Cell Communication; D002454:Cell Differentiation; D016207:Cytokines / Q000276:immunology / Q000378:metabolism; D006801:Humans; D008168:Lung / Q000276:immunology* / Q000378:metabolism / Q000821:virology; D008213:Lymphocyte Activation; D010641:Phenotype; D018357:Respiratory Syncytial Virus Infections / Q000276:immunology* / Q000378:metabolism / Q000517:prevention & control / Q000821:virology; D022261:Respiratory Syncytial Virus Vaccines / Q000276:immunology; D012136:Respiratory Syncytial Viruses / Q000276:immunology* / Q000378:metabolism / Q000472:pathogenicity; D015398:Signal Transduction; D050378:T-Lymphocytes, Regulatory / Q000276:immunology* / Q000378:metabolism / Q000821:virology; D058504:Th17 Cells / Q000276:immunology* / Q000378:metabolism / Q000821:virology
D016207:Cytokines; D022261:Respiratory Syncytial Virus Vaccines