Immune cells called T cells are guilty of detecting pathogens, killing inflamed cells, and recruiting other branches of the immune formula to fight infection.
However, according to the new study, T mobile’s responses to the new coronavirus in critical patients appear to be as physically powerful as those with a milder form of the disease.
The discovery reinforces the conclusion that an insufficient immune reaction to SARS-CoV-2, the coronavirus that causes COVID-19, is not guilty of serious illness and death, but is to blame for an exaggerated immune reaction.
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The study team, led by the Marien De Herne Hospital and the Ruhr-University Bochum in Herne, Germany, compared the T-cell responses of 28 COVID-19 patients in the acute phase of infection and then curative in survivors. .
Of these infections, 7 were classified as moderate, 9 serious and 12 critical.
The scientists measured the concentration of two types of T cells in samples of the patient’s blood: helper T cells and killer or “cytotoxic” T cells.
They also analyzed the strength of these cells’ responses to 3 different portions of the virus: the 3 proteins that make up its peaks, its membrane, and the layer or “nucleocapsid” that surrounds its nuclear material.
In addition, they measured the degrees of cytokines (immune signaling molecules) that T cells produce to fight infections.
They found that in patients with a serious illness, the scale of their immune responses is similar or even larger, compared to moderate or severe cases.
There is also no obvious trade-off between successful virus clearance or death and adjustments in T cell responses.
“The total number of express immune cells and their functionality is no greater in patients who survived COVID-19 than in those who died from it,” explains Dr. Ulrik Stervbo, one of the authors.
It’s in Cell Reports Medicine magazine.
T cells migrate to a viral infection site, kill inflamed cells, and settle into other portions of the immune formula to neutralize the virus.
But those same T cells can also create a “cytokine storm,” which is for a life-threatening complication known as acute respiratory distress syndrome (EDS).
“While additional studies will be needed to perceive the express mechanism of progression of COVID-19, our knowledge recommends that the superior reaction of T cells expressing SARS-CoV-2 would possibly cause [immune damage] leading to COVID-19. – related lung failure, “says lead professor Nina Babel.
The new studies add to a developing evidence framework that higher immune responses cause life-threatening COVID-19.
A primary published in June 2020 found that dexamethasone, a corticosteroid that suppresses the body’s immune response, stored the life of about a third of all ventilator patients for a period of 28 days.
A more recent study, published via Medical News Today, suggests that some other type of immunosuppressive drug, known as an interleukin-6 inhibitor, could possibly prevent serious COVID-19 infections from being life-threatening.
The authors of the new one recognize some limitations of their research.
They don’t know exactly when patients in their studies contracted the virus. Therefore, the reaction of higher T cells in critically ill patients would possibly only result from a longer era of infection.
Furthermore, they were unable to analyze the full diversity of T-cell subtypes and the cytokines they produce, so they possibly would have missed the protective or destructive immune effects that other effects had on critical and non-critical patients. .
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