Severe COVID-19 linked to overactive immune cells, study says

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Samples from the lungs of patients show a runaway immune system reaction could be one mechanism behind severe novel coronavirus (COVID-19) cases, according to a new study led by Imperial College London and published in the journal Frontiers in Immunology.

When we are infected with pathogens like bacteria and viruses, our bodies mount several types of immune system response. One of the major components are T cells, which come in several different forms that coordinate the immune response, from killing infected cells to recruiting more T cells to the fight, the researchers said.

Sometimes, our immune system overreacts to invaders, for example during an allergic reaction, resulting in T cells killing normal, healthy cells and causing tissue damage. However, there is a brake mechanism that should kick in, causing T cells to reduce their activity and calming inflammation, said the researchers.

The researchers tested samples from the lungs of six COVID-19 patients in China with severe symptoms and compared them to samples from three moderate COVID-19 patients and three healthy individuals. Although the samples were from relatively few patients, the researchers investigated gene usage in single cells, gaining fine detail on the immune system response. This method allowed them to analyze rare cells and their dynamics, which cannot be achieved with conventional methods, according to the study.  

The study found that the lungs of severe COVID-19 patients had accumulated a broad range of 'hyperactivated' T cells, suggesting the brake mechanism had failed. This overreaction paralyses the overall T cell system, causing it to fail at fighting the virus, as well as causing more damage to the lungs through severe inflammation and tissue destruction, the researchers said.

On closer inspection of the mechanism, the researchers said they found that the protein Foxp3, which usually induced the brake mechanism, is inhibited in lungs of severe COVID-19 patients. They are unsure why Foxp3 is inhibited, but further research could reveal this, and potentially lead to a way to put the brakes back on the T cell response, reducing the severity of the disease.

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