Consistent abrogation of T(H)2 response to HDM and influenza was observed with IFN-β at both time points; attenuation was observed by day 5 with RV and TT.
Specific activation of RLR in moDCs by poly(I:C) or influenza virus was shown to induce the secretion of IFN-β via IRF3, whereas induction of proinflammatory cytokine responses were predominantly controlled by TLR3.
Influenza virus infected cells treated with representative HuScFv (clone 10) had up-expression of IRF3 and IFN-β genes by 14.75 and 4.95-fold, respectively, in comparison with the controls, indicating that the antibodies could restore the host innate immune response.
In this cohort of pre-school asthmatic children, nasopharyngeal colonization with Gram-negative bacteria such as Haemophilus influenzae and Moraxella catarrhalis was found to be associated with the highest interferon beta (IFNβ) and IL-33 levels in the nasal pharyngeal fluids (NPF).
It was found that ethanol and water crude extracts of C. longa and K. parviflora induced significant upregulation of TNF-α and IFN-β mRNA expressions, suggesting their roles in the inhibition of H5N1 virus replication.
Long-term exposure to PM2.5 lowers influenza virus resistance via down-regulating pulmonary macrophage Kdm6a and mediates histones modification in IL-6 and IFN-β promoter regions.
Strikingly no differences were observed between these two groups, while plasma from acute influenza infection revealed significantly higher plasma levels of both IFNα and IFNβ proteins.