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Journal of Cellular Immunology

ISSN: 2689-2812

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

Gregory V Plano1, Noula Shembade1,*
  • 1Department of Microbiology and Immunology, Sylvester Comprehensive Cancer Center Miller School of Medicine, University of Miami, Miami, FL 33136, USA
+ Affiliations - Affiliations

Corresponding Author

Noula Shembade, nshembade@med.miami.edu

Received Date: November 21, 2020

Accepted Date: February 02, 2021

Citation:

Plano G, Shembade N. Role of Perforin-2 in Regulating Type I Interferon Signaling. J Cell Immunol. 2021; 3(1): 53-60.


Copyright: © 2021 Plano G, et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.

Abstract

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.

Keywords

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

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Role of Perforin-2 in Regulating Type I Interferon Signaling

Type I interferons (IFNs) produced in response to infections with either bacterial, viral or fungal pathogens are critical to induce antimicrobial defenses in infected and adjacent cells to reduce the spread of microbes, initiate communication between innate and adaptive immunity, and to promote the survival of the host [1]. Improper induction or regulation of type I IFN signaling can lead to chronic infection-induced inflammation-related diseases, including septic shock, autoimmune diseases, and inflammatory syndromes [2].

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