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Mutual regulations between and type I interferon. | LitMetric

Mutual regulations between and type I interferon.

Front Immunol

Department of Microbiology and Parasitology, Anhui Province Laboratory of Zoonoses, School of Basic Medical Sciences, Anhui Medical University, Hefei, Anhui, China.

Published: July 2024

AI Article Synopsis

  • Type I interferon (IFN-I) has been extensively researched for its antiviral properties but is now recognized for its role in infections caused by a specific intracellular parasite.
  • The production and effect of IFN-I are influenced by various factors, including the type of cells involved, the strain of the parasite, and the genetic makeup of the mouse model used.
  • The article highlights how both IFN-I and the parasite interact, with the parasite potentially using certain proteins to manipulate the IFN-I response, pointing towards new avenues for therapeutic interventions.

Article Abstract

In the decades since the discovery, Type I interferon (IFN-I) has been intensively studied for their antiviral activity. However, increasing evidences suggest that it may also play an important role in the infection of , a model organism for intracellular parasites. Recent studies demonstrated that the induction of IFN-I by the parasite depends on cell type, strain genotype, and mouse strain. IFN-I can inhibit the proliferation of , but few studies showed that it is beneficial to the growth of the parasite. Meanwhile, also can secrete proteins that impact the pathway of IFN-I production and downstream induced interferon-stimulated genes (ISGs) regulation, thereby escaping immune destruction by the host. This article reviews the major findings and progress in the production, function, and regulation of IFN-I during infection, to thoroughly understand the innate immune mechanism of infection, which provides a new target for subsequent intervention and treatment.

Download full-text PDF

Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC11260619PMC
http://dx.doi.org/10.3389/fimmu.2024.1428232DOI Listing

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