tetano
Editor, Senior Moderator
Immunol Cell Biol. 2016 Sep 15. doi: 10.1038/icb.2016.91. [Epub ahead of print]
[h=1]Differential Mucosal IL-10-induced immunoregulation of innate immune responses occurs in influenza infected infants/toddlers and adults.[/h] Verhoeven D[SUP]1,[/SUP][SUP]2[/SUP], Perry S[SUP]1[/SUP].
[h=3]Author information[/h]
[h=3]Abstract[/h] Young children (<5 years of age but especially those <2 years old) exhibit high rates of morbidity and frequently require hospitalizations due to complications from respiratory viral infections. This is also a population for which we understand less about how their unique level of immunological maturation affects their antiviral immune responses. However, we do know from prior studies that their T-cells appear to apoptose in the lungs due to limited IFNγ autocrine signaling during infection. To begin to further understand additional limits, we utilized an infant/toddler murine model infected with influenza virus with an adult comparator. In our model, young mice exhibited lower IL-10[SUP]+[/SUP]IFNγ[SUP]+[/SUP] co-producing CD4 T-cells infiltrating the lungs that paralleled with a failed switch from an innate to adaptive immune response at the mid infection stage. Specifically, limited co-IL-10 production correlated with a lack of influenza-specific antibodies and subsequent complement receptor signaling (CRRY/p65) to the lung infiltrating CD4 T-cells therefore limiting their IKAROs up-regulation. Thus, limited IL-10 production appeared to diminish signaling to lung macrophages to stop accumulating late into infection. Taken together, our results suggest a novel role for complement mediated signaling in CD4 T-cells with respect to IL-10 co-production. Furthermore, a subsequent failure to shift from the unfocused innate immune response to the specific adaptive responses may be a principle cause in the enhanced morbidity common in respiratory viral infection of young children.Immunology and Cell Biology accepted article preview online, 15 September 2016. doi:10.1038/icb.2016.91.
PMID: 27629065 DOI: 10.1038/icb.2016.91
[PubMed - as supplied by publisher]
[h=1]Differential Mucosal IL-10-induced immunoregulation of innate immune responses occurs in influenza infected infants/toddlers and adults.[/h] Verhoeven D[SUP]1,[/SUP][SUP]2[/SUP], Perry S[SUP]1[/SUP].
[h=3]Author information[/h]
[h=3]Abstract[/h] Young children (<5 years of age but especially those <2 years old) exhibit high rates of morbidity and frequently require hospitalizations due to complications from respiratory viral infections. This is also a population for which we understand less about how their unique level of immunological maturation affects their antiviral immune responses. However, we do know from prior studies that their T-cells appear to apoptose in the lungs due to limited IFNγ autocrine signaling during infection. To begin to further understand additional limits, we utilized an infant/toddler murine model infected with influenza virus with an adult comparator. In our model, young mice exhibited lower IL-10[SUP]+[/SUP]IFNγ[SUP]+[/SUP] co-producing CD4 T-cells infiltrating the lungs that paralleled with a failed switch from an innate to adaptive immune response at the mid infection stage. Specifically, limited co-IL-10 production correlated with a lack of influenza-specific antibodies and subsequent complement receptor signaling (CRRY/p65) to the lung infiltrating CD4 T-cells therefore limiting their IKAROs up-regulation. Thus, limited IL-10 production appeared to diminish signaling to lung macrophages to stop accumulating late into infection. Taken together, our results suggest a novel role for complement mediated signaling in CD4 T-cells with respect to IL-10 co-production. Furthermore, a subsequent failure to shift from the unfocused innate immune response to the specific adaptive responses may be a principle cause in the enhanced morbidity common in respiratory viral infection of young children.Immunology and Cell Biology accepted article preview online, 15 September 2016. doi:10.1038/icb.2016.91.
PMID: 27629065 DOI: 10.1038/icb.2016.91
[PubMed - as supplied by publisher]