A critical role of IL-17 in modulating the B-cell response during H5N1 influenza virus infection. The 107 challenge dose we used was in line with other human and experimental influenza challenge studies. For the repertoire analysis, because chi-square tests were not applicable due to the presence of zero-values in contingency table cells, statistical association across treatment conditions was assessed using Fisher’s exact test as implemented in R (. Impact of respiratory virus infections on persons with chronic underlying conditions. 2017, SYK-CARD9 Signaling Axis Promotes Gut Fungi-Mediated Inflammasome Activation to Restrict Colitis and Colon Cancer, Antibodies Set Boundaries Limiting Microbial Metabolite Penetration and the Resultant Mammalian Host Response, γδ T Cells Protect Neonatal Mice against Influenza Infection by Promoting Tissue Restoration Independent of Viral Clearance, γδ T Cells Protect Neonatal Mice against Influenza Infection via Promotion of Lung Homeostasis and Repair, Independent of Viral Clearance, γδ T Cells Rapidly Produce IL-17A after Neonatal Influenza Infection, IL-17A-Producing γδ T Cells Rapidly Accumulate and Respond to Influenza Infection in Neonatal Mice, IL-17A, Primarily Secreted by γδ T Cells, Improves the Survival of Influenza-Infected Neonates by Enhancing IL-33 Production, IL-17A, Predominantly Secreted by γδ T Cells, Improves the Survival of Influenza-Infected Neonates by Promoting IL-33 Production, IL-17A Promotes IL-33 Production in Mouse Lung Epithelial Cells in Synergy with Influenza Virus by Elevating STAT3 Phosphorylation, IL-17A Elevates IL-33 Production in Murine Lung Epithelial Cells via STAT3 Phosphorylation, Deficiency in γδ T Cells Compromises the Accumulation and Functions of ILC2s and Treg Cells, Deficiency in γδ T Cells Results in Decreased Accumulation and Functionality of ILC2s and Treg Cells, IL-17A, IL-33, and Areg Are Correlated with Each Other and with Improved Outcomes in Influenza-Infected Human Children, The IL-17A/IL-33/Areg Cascade in Influenza-Infected Children Is Associated with Robust Disease Outcome, Ethical Compliance for Mouse and Human Studies, Quantification of IAV in Infected Lung Tissue, Cytokine Measurement of Mouse Lung Homogenates, We use cookies to help provide and enhance our service and tailor content and ads. Probable person-to-person transmission of avian influenza A (H5N1). This 50% protective titer is defined for each age group a ∈ {child, adult}, \({\mathrm{TP50}}_{a_i,s}\) (Eq. 2) implies that most individuals (i.e., even individuals with titer <10, the lower limit of detection by HI assays) benefit from minor additional protection after infection. For individuals younger than 12 years old during the year of observation, the probability that an individual was naive in observation year y is. Further information and requests for resources and reagents should be directed to and will be fulfilled by the Lead Contact, P.G. Recent studies implicate commensal bacteria in the innate priming of adaptive antiviral immune responses to influenza virus. bSerum antibody titers against the hemagglutinin head, NAI, and HA stalk were measured at D0 and at W8. Approaching the asymptote?
Toll-like receptor expression in murine DC subsets: lack of TLR7 expression by CD8α+ DC correlates with unresponsiveness to imidazoquinolines. From the latent infections and susceptibility for each individual, we track the loss of protection after infection. J. Infect. Innate immune cytokines, such as IL-1 (Refs 41, 54, 55), IL-6 (Ref. Miller, M. S. et al.
Chang, Y. J. et al. Commensal bacteria calibrate the activation threshold of innate antiviral immunity.
What protection does a flu vaccine provide if I do get sick with flu? Google Scholar. Dis.
Influenza virus-induced type I interferon leads to polyclonal B-cell activation but does not break down B-cell tolerance. For each participant, gene expression analysis was performed by expression microarray, and gene expression on days post–viral challenge was normalized to each participant’s baseline (day 0) expression values.
Black, S. et al. Biol. For neonatal EdU experiments, infected neonates were injected intraperitoneally (i.p.) The study protocol was approved by the Institutional Review Board of the University of Hong Kong. Freeman, G. et al. In this Review, we discuss the various ways in which the innate immune system uses pattern recognition receptors to detect and respond to influenza virus infection. has received research funding from Sanofi, and honoraria from Sanofi and Roche. 27, 229–265 (2009). These authors contributed equally: Benjamin J. Cowling, Sarah Cobey. Identifying correlates of protection against human influenza A virus infection is a necessary step in developing more broadly protective (“universal”) influenza vaccines [1]. PLoS Pathog.
Coudeville, L. et al. If infection following a high-dose viral challenge does not raise fully protective homotypic immunity, can we expect vaccines to be made that will do so, let alone provide heterologous protection? In addition to type I IFNs, IFNγ (the type II IFN) and IFNλ (a member of the type III IFN family) contribute to innate antiviral defence. It is likely that strategies may need to be employed that target multiple viral antigens to produce new generations of influenza vaccines that induce strong and durable protection. Immunity 30, 566–575 (2009).
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