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
"Don’t Eat Me” Study Could Lead to Broad-spectrum Infectious Diseases Immunotherapy
News

"Don’t Eat Me” Study Could Lead to Broad-spectrum Infectious Diseases Immunotherapy

"Don’t Eat Me” Study Could Lead to Broad-spectrum Infectious Diseases Immunotherapy
News

"Don’t Eat Me” Study Could Lead to Broad-spectrum Infectious Diseases Immunotherapy

Colorized scanning electron micrograph of a cell (purple) infected with SARS-CoV-2 virus particles (yellow), isolated from a patient sample. Credit: NIAID
Read time:
 

Want a FREE PDF version of This News Story?

Complete the form below and we will email you a PDF version of ""Don’t Eat Me” Study Could Lead to Broad-spectrum Infectious Diseases Immunotherapy"

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

National Institutes of Health investigators and colleagues have discovered that when the immune system first responds to infectious agents such as viruses or bacteria, a natural brake on the response prevents overactivation. Their new study in mBio describes this brake and the way pathogens such as SARS-CoV-2, the virus that causes COVID-19, turn it on. Their finding provides a potential target for an immunotherapy that might be applied to a wide range of infectious diseases.

When a cell senses an infectious agent with molecules called pathogen recognition receptors, part of its response is to increase cell surface expression of a molecule called CD47, otherwise known as the “don’t eat me” signal. Increased CD47 expression dampens the ability of cells called macrophages, the immune system’s first responders, to engulf infected cells and further stimulate the immune response. Upregulation of CD47 on cells was observed for diverse types of infections including those caused by mouse retroviruses, lymphocytic choriomeningitis virus, LaCrosse virus, SARS CoV-2, and by the bacteria Borrelia burgdorferi and Salmonella enterica typhi.

By blocking CD47-mediated signaling with antibodies in mice infected with lymphocytic choriomeningitis virus, the authors demonstrated they could enhance the speed of pathogen clearance. Furthermore, knocking out the CD47 gene in mice improved their ability to control M. tuberculosis infections and significantly prolonged their survival. In addition, retrospective studies of cells and plasma from people infected with hepatitis C virus indicated that humans also upregulate CD47.  In these studies, inflammatory cytokine stimuli and direct infection both promoted increased CD47 expression.

This highly collaborative research project involved 14 different institutions and was led by scientists from NIH’s National Institute of Allergy and Infectious Diseases in Hamilton, Montana, and Stanford University in Stanford, California. The findings open the possibility of using CD47 blockade as a new immunotherapeutic to treat a wide range of different infections. “There may be circumstances where host responses need boosting and CD47 represents a novel target for host-directed therapies in such cases,” the scientists write, mentioning SARS-CoV-2, HIV, HPV and Ebola virus among several possibilities.

Reference


Tal et al. (2020). Upregulation of CD47 Is a Host Checkpoint Response to Pathogen Recognition. mBio. DOI: https://doi.org/10.1128/mBio.01293-20

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

Advertisement