The role of Th17 and Treg responses in the pathogenesis of RSV infection

Mangodt, Thomas C.; Herck, Mikhaïl A. Van; Nullens, Sara; Ramet, José; Dooy, Jozef J. De; Winter, Benedicte Y. De

doi:10.1038/pr.2015.143

Cited by 82 publications

(95 citation statements)

References 94 publications

(150 reference statements)

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“…The high levels of IL-6 observed in the airways of infants with a primary RSV infection would favor differentiation of a proportion of lymphocytes toward an IL-17-producing phenotype. A recent review (36) concluded that data from studies involving RSV-infected infants as well as animal models and in-vitro work with RSV-infected epithelium supported this suggestion. The potential role of Articles TH17 cells in contributing to protection against repeated infection was also highlighted in a study which demonstrated that the RSV NS1protein, which acts as an interferon antagonist, specifically suppresses proliferation and activation of both CD103+CD8+ cells and TH17 cells (37).…”

Section: Discussionmentioning

confidence: 99%

Cytokine responses in primary and secondary respiratory syncytial virus infections

et al. 2016

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Background: Primary respiratory syncytial virus (RSV) infections are characterized by high levels of IL-8 and an intense neutrophilia. Little is known about the cytokine responses in secondary infections. Preschool children experiencing RSV secondary infections were recruited from the siblings of infants admitted to hospital with RSV acute bronchiolitis. Methods: Fifty-one infants with acute bronchiolitis (39 RSV positive, 12 RSV negative) and 20 age-matched control infants were recruited. In addition, seven older siblings of infants from the RSV-positive cohort and confirmed RSV infection were recruited. Samples of nasal secretions were obtained using a flocked swab, and secretions extracted using centrifugation. Cytokine bead array was used to obtain levels of interleukin (IL)-17A, IL-8, IL-6, IL-21, and tumor necrosis factor-α. results: Levels of IL-8 and IL-6 were significantly lower in the RSV-positive siblings compared with the RSV-positive infants. There were no significant differences between levels of the other cytokines in the primary and secondary infections. conclusion: The very high levels of IL-8 and IL-6 response characteristic of the primary RSV infection was not observed in secondary RSV-positive infections and this did not appear to be due to a global reduction in cytokine production.

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Section: Discussionmentioning

confidence: 99%

Cytokine responses in primary and secondary respiratory syncytial virus infections

et al. 2016

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“…In contrast, if the T cell responses are skewed towards a Th2 type, they can contribute to immunopathology 62, 93– 95 . Although, more recently, some of these observations have also been attributed to Th17 induction 96 .…”

Section: Adaptive Immune Responses To Rsvmentioning

confidence: 99%

Respiratory syncytial virus infection: an innate perspective

Johansson

2016

F1000Res

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Respiratory syncytial virus (RSV) is a common cause of upper respiratory tract infection in children and adults. However, infection with this virus sometimes leads to severe lower respiratory disease and is the major cause of infant hospitalisations in the developed world. Several risk factors such as baby prematurity and congenital heart disease are known to predispose towards severe disease but previously healthy, full-term infants can also develop bronchiolitis and viral pneumonia during RSV infection. The causes of severe disease are not fully understood but may include dysregulation of the immune response to the virus, resulting in excessive recruitment and activation of innate and adaptive immune cells that can cause damage. This review highlights recent discoveries on the balancing act of immune-mediated virus clearance versus immunopathology during RSV infection.

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“…Notably, many CD4 T-cell-specific cytokines have been detected and implicated in human RSV-induced disease (12–14). In mice, RSV-induced disease has been shown to be mediated by an improper skewing of CD4 T cell subsets (9, 15, 16). T helper (Th) 1 polarized CD4 T cells that produce IFN-γ and TNF-α contribute to the clearance of viral infections, however, RSV infection often induces both Th2 and Th17 responses (16–18).…”

Section: Introductionmentioning

confidence: 99%

Altered Treg and cytokine responses in RSV-infected infants

et al. 2016

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Background: Respiratory syncytial virus (RSV) is the leading cause of bronchiolitis and pneumonia in children under one year of age in the United States. The host immune response is believed to contribute to RSV-induced disease. We hypothesize that severe RSV infection in infants is mediated by insufficient regulation of the host immune response of regulatory T cells (Tregs) resulting in immunopathology. Methods: Blood and nasal aspirates from 23 RSV-infected and 17 control infants under 1 year of age were collected. Treg frequencies were determined by flow cytometry from peripheral blood mononuclear cells. Analysis of 24 cytokines was measured by multiplex assay on nasal aspirates. Results: We demonstrate that the frequency of activated Tregs is significantly reduced in the peripheral blood of RSV-infected infants compared to age-matched controls. Surprisingly, Th17 related cytokines including IL-1β, IL-17A, and IL-23 were associated with a reduction in clinical symptoms of respiratory distress. In addition, the amount of IL-33 protein in nasal washes, a cytokine important in maintaining Treg homeostasis in mucosal tissues, was decreased in RSV-infected children. Conclusion: These results suggest that decreased Treg numbers and an inability to properly control the host inflammatory response results in severe RSV infection.

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The role of Th17 and Treg responses in the pathogenesis of RSV infection

Cited by 82 publications

References 94 publications

Cytokine responses in primary and secondary respiratory syncytial virus infections

Cytokine responses in primary and secondary respiratory syncytial virus infections

Respiratory syncytial virus infection: an innate perspective

Altered Treg and cytokine responses in RSV-infected infants

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