We've updated our Privacy Policy to make it clearer how we use your personal data.

We use cookies to provide you with a better experience. You can read our Cookie Policy here.

Advertisement
How Viruses Disarm the Immune System
News

How Viruses Disarm the Immune System

How Viruses Disarm the Immune System
News

How Viruses Disarm the Immune System

Credit: McGill University.
Read time:
 

Want a FREE PDF version of This News Story?

Complete the form below and we will email you a PDF version of "How Viruses Disarm the Immune System"

First Name*
Last Name*
Email Address*
Country*
Company Type*
Job Function*
Would you like to receive further email communication from Technology Networks?

Technology Networks Ltd. needs the contact information you provide to us to contact you about our products and services. You may unsubscribe from these communications at any time. For information on how to unsubscribe, as well as our privacy practices and commitment to protecting your privacy, check out our Privacy Policy

How do viruses that cause chronic infections, such as HIV or hepatitis C virus, manage to outsmart their hosts’ immune systems?

The answer to that question has long eluded scientists, but new research from McGill University has uncovered a molecular mechanism that may be a key piece of the puzzle. The discovery could provide new targets for treating a wide range of diseases.


Fighting off infections depends largely on our bodies’ capacity to quickly recognize infected cells and destroy them, a job carried out by a class of immune cells known as CD8+ T cells. These soldiers get some of their orders from chemical mediators known as cytokines that make them more or less responsive to outside threats. In most cases, CD8+ T cells quickly recognize and destroy infected cells to prevent the infection from spreading.  


“When it comes to viruses that lead to chronic infection, immune cells receive the wrong set of marching orders, which makes them less responsive,” says Martin Richer, an assistant professor at McGill’s Department of Microbiology & Immunology and senior author of the study, published recently in the journal Immunity.


The research, conducted in Richer’s lab by graduate student Logan Smith, revealed that certain viruses persist by driving the production of a cytokine that leads to modification of glycoproteins on the surface of the CD8+ T cells, making the cells less functional. That maneuver buys time for the pathogen to outpace the immune response and establish a chronic infection. Importantly, this pathway can be targeted to restore some functionality to the T cells and enhance the capacity to control infection.


The discovery of this regulatory pathway could help identify new therapeutic targets for a variety of diseases. “We might be able to take advantage of the pathways induced by these signals to fight chronic viral infections by making the immune system more responsive,” Richer says. “The findings might also prove useful for diseases like cancer and autoimmunity, where T cells function is poorly regulated.”

This article has been republished from materials provided by McGill University. Note: material may have been edited for length and content. For further information, please contact the cited source.

Reference

Interleukin-10 Directly Inhibits CD8+ T Cell Function by Enhancing N-Glycan Branching to Decrease Antigen Sensitivity. Logan K. Smith, Giselle M. Boukhaled, Stephanie A. Condotta, Sabrina Mazouz, Jenna J. Guthmiller, Rahul Vijay, Noah S. Butler, Julie Bruneau, Naglaa H. Shoukry, Connie M. Krawczyk, Martin J. Richer. Immunity In Press DOI: https://doi.org/10.1016/j.immuni.2018.01.006.


Advertisement