Review Article Open Access
Volume 3 | Issue 1 | DOI: https://doi.org/10.33696/immunology.3.078

Role of Perforin-2 in Regulating Type I Interferon Signaling

  • 1Department of Microbiology and Immunology, Sylvester Comprehensive Cancer Center Miller School of Medicine, University of Miami, Miami, FL 33136, USA
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Corresponding Author

Noula Shembade, nshembade@med.miami.edu

Received Date: November 21, 2020

Accepted Date: February 02, 2021


Sepsis is a systemic inflammatory response caused by a harmful host immune reaction that is activated in response to microbial infections. Infection-induced type I interferons (IFNs) play critical roles during septic shock. Type I IFNs initiate their biological effects by binding to their transmembrane interferon receptors and initiating the phosphorylation and activation of tyrosine kinases TYK2 and JAK1, which promote phosphorylation and activation of STAT molecules. Type I IFN-induced activation of JAK/STAT pathways is a complex process and not well understood. Improper regulation of type I IFN responses can lead to the development of infectious and inflammation-related diseases, including septic shock, autoimmune diseases, and inflammatory syndromes. This review is mainly focused on the possible mechanistic roles of the transmembrane Perforin-2 molecule in the regulation of type I IFNinduced signaling.


JAK/STAT, Interferons, TYK2, STATs, Perforin-2, IFNAR1, IFNAR2 and Signaling

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