Date: April 23, 2024 By: Nick Kolev
A collaborative research study led by Ragon Institute faculty member and Early Independence fellow Wilfredo F. Garcia-Beltran, MD, PhD, and Ragon Biosafety Level 3 Core co-director Julie Boucau, PhD, has uncovered a critical mechanism by which SARS-CoV-2 evades one of the body’s key immune responses, providing new insights that could lead to novel treatments.
Their findings, to be published in Cell next month, reveal how the virus manipulates immune system processes to avoid destruction by natural killer (NK) cells, a type of white blood cell that is crucial for fighting viral infections.
“NK cells serve as a first-line defense against viruses like SARS-CoV-2 and learning how this virus is able to overcome the human body’s first defenses is a huge breakthrough that can help us prevent and treat future viral outbreaks,” Garcia-Beltran said.
The virus achieves this stealth by interfering with the NKG2D receptor on NK cells. Normally, this receptor helps the immune system detect and destroy infected cells by recognizing certain stress signals on their surface. SARS-CoV-2 reduces these signals through a process known as “shedding,” making infected cells nearly invisible to immune defenses.
The researchers identified a monoclonal antibody in pre-clinical studies against cancer, called 7C6, that can block this shedding process, making the infected cells more visible again to NK cells. This discovery could lead to new treatments that enhance the immune system’s ability to fight the virus, potentially boosting the effectiveness of existing COVID-19 vaccines and therapies.
By using advanced techniques to explore these interactions, the team has opened new avenues for treatment strategies that could also be relevant for tackling future viral outbreaks.
Researchers at the Ragon Institute of Mass General Brigham, MIT, and Harvard have uncovered critical insights into how aging impairs the immune system’s ability to fight cancer.
This study, published in Immunity on August 30, used a non-human primate model to demonstrate that previous Mtb infection leads to a durable, protective immune response that is dependent on CD4+ T cells.
MIT researchers find that the first dose primes the immune system, helping it to generate a strong response to the second dose, a week later.