Signaling Protein Tpl2 That Regulates Interferons Is Key to Immune Defense Against Influenza Infection; Tpl2 Knockout Mice Show 10-Fold Higher Influenza Virus Titers, Decreased Cytotoxic T-Cell Numbers, & Reduced Levels of Type III Interferons

Infectious disease researchers at the University of Georgia (UGA) have identified a signaling protein critical for host defense against influenza infection. The findings, published on xxxxxx in the open-access journal PLOS Pathogens, shed light on how a single component of the body's defense system promotes effective immunity against viral infections, particularly respiratory viruses that affect mucosal sites. The new article is titled “Tumor Progression Locus 2 Promotes Induction of IFNλ, Interferon-Stimulated Genes, and Antigen-Specific CD8+ T Cell Responses and Protects Against Influenza Virus.” The tumor progression locus 2 protein (Tpl2) is an important regulator of the immune response, controlling signaling downstream of cell-surface and intracellular receptors that recognize the presence of pathogens. Tpl2 regulates the production of a group of immune signaling proteins called interferons. Though interferon production is known to play a large role in host defense against viral infections, prior to this study little was known about how Tpl2 functions in that environment. The new study demonstrates a key role for Tpl2 in induction of anti-viral genes, including those for Type III interferons, a type of immune signaling protein, important in mediating antiviral responses. "Tpl2 regulates inflammation and inflammation is a necessary part of a host's defense against infection," said Wendy Watford (photo), Ph.D. (from Duke University), corresponding author on the study and an Associate Professor of Infectious Diseases in the UGA College of Veterinary Medicine. Ongoing projects in Dr. Watford's lab seek to understand how Tpl2 modulates the host immune response in different disease settings.
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