A group of scientists at Stony Brook University has discovered a new role for retinoic acid, a metabolite of vitamin A, during the immune response of the gut.
This finding could lead to ways to control the retinoic acid response and therefore be used as a therapy or for vaccine development against infection or even to treat gastrointestinal (GI) tumors.
The study examined the factors that control the generation of cytotoxic memory CD8 T cells, which are an important arm of the body’s anti-pathogen immune response.
Memory CD8 T cells provide long-lived and frontline protection at barrier tissues, highlighting their importance in vaccine design.
To date, scientists have known that retinoic acid in the gut-draining lymph nodes promotes effector CD8 T cell migration to the intestines, enhancing the immune response.
Additionally, vitamin A deficiency is associated with increased infections and poor vaccine efficiency.
The team found a new role for retinoic acid, which is a key part of the immune process in the gut.
They demonstrated in the lab that T cell activation in gut-associated lymph nodes regulates memory CD8 T cell differentiation in the intestine.
They also demonstrated that T cells activated at other sites were impaired in the ability to differentiate into memory CD8 T cells after entry into the intestine.
During this process, they showed that activation within the gut-associated lymph nodes, but not in other sites, promotes intestinal memory CD8 T cell development and that retinoic acid signals provided during this window of T cell activation in the lymph nodes enhance intestinal memory CD8 T cell development to a wider degree.
The study highlights a fundamental new role of T cell activation on the generation of the intestinal memory CD8 T cells that appears distinct from other barrier sites like the lungs and skin.
The research team was able to replicate this limiting or promoting of retinoic acid signals in the gut.
They believe that manipulating retinoic acid signals during T cell activation may provide a strategy for clinicians to promote or limit intestinal CD8 T cells to improve vaccine outcomes or limit immunopathology.
In summary, the study shows that retinoic acid plays a vital role in the immune response of the gut and could potentially be used as a therapy or for vaccine development against infections or GI tumors.
By manipulating retinoic acid signals during T-cell activation, clinicians may be able to improve vaccine outcomes or limit immunopathology.
Gut infection, also known as gastroenteritis, is a medical condition that causes inflammation in the lining of the digestive tract.
The infection is usually caused by viruses, bacteria, or parasites that are ingested through contaminated food or water, or by coming into contact with infected individuals.
Symptoms of gut infection include diarrhea, vomiting, nausea, abdominal pain, cramps, and fever. These symptoms can range from mild to severe and can last from a few days to several weeks.
Gut infection can be diagnosed through a stool sample test that detects the presence of the infectious agent in the digestive system.
Treatment typically involves resting, drinking plenty of fluids, and avoiding solid foods until symptoms improve.
In some cases, medication may be prescribed to alleviate symptoms or to target the specific cause of the infection.
Prevention of gut infection can be done by practicing good hygiene, such as washing hands regularly, especially before preparing or eating food, avoiding contaminated food and water, and properly storing and cooking food.
In addition, vaccines are available for certain types of gut infections, such as rotavirus, which is a common cause of diarrhea in young children.
If you care about nutrition, please read studies that eating nuts may help reduce risks of the gut lesion and cancer, and how tea and coffee influence your risk of high blood pressure.
For more information about nutrition, please see recent studies that anti-inflammatory diet could help prevent fatty liver disease, and vitamin D could help lower the risk of autoimmune diseases.
The study was conducted by Brian Sheridan et al and published in the Journal of Experimental Medicine.
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