In the early stages of the COVID-19 pandemic, many immunologists believe that patients who produce large amounts of antibodies in the early stages of infection may not get sick, but this may not be the case. no. After studying COVID-19 for a few months, researchers believe that the situation of COVID-19 infection may be more complicated than you think. Recent studies have shown that in some patients, preventing immune system disorders is as important as treating viral infections.
Today, people are increasingly aware that the power of the immune system to fight infection may be insignificant, and the emergence of the COVID-19 pandemic is also a painful turning point. In addition to having antiviral capabilities, in patients with severe COVID-19, the inflammatory process used to fight SARS-CoV-2 will also harm the patient. In clinical studies, researchers explained the so-called cytokine storm. Children who have recovered from COVID-19 have many inflammatory molecules and antibodies, which can induce dangerous thrombosis and formation in multiple organ systems including blood vessels. Symptoms of inflammation. sexual. These are signs of danger. In some patients, the body is opposed to SARS-CoV-2 and the immune response may have shifted from a healing gradient to a destructive gradient. Hope to understand
The characteristics of the immune system diseases of COVID-19 patients help to identify which patients can benefit the most from treatment and retain autoimmune diseases. It may be correct to prove that the current powerful methods for regulating the immune system are more targeted. Antibodies are powerful weapons, produced by white blood cells called B cells. It can capture infectious agents such as viruses and bacteria, and effectively prevent infection of healthy cells. These antibody-virus aggregates have a strong release ability. As a homing signal, the inflammatory response (and in some cases death) can effectively trap pathogens in the body's other frontal immune systems. Antibodies are so powerful that they may accidentally cause extensive organ damage to the body. You can also establish a permanent immune self-targeting cycle. This self-destructive state can be called an autoimmune disease. B cells need to be trained to avoid autoimmune diseases and ensure an effective immune response against invading pathogens. B cells that respond to the virus will improve their antibodies and continue to mature. To ensure that potential antibodies can inactivate invaders. However, this maturation process takes time. During severe infections, the body needs a faster antibody response, because two weeks of B cell training can mean the difference between life and death. To fill this gap, the immune system has produced another form of B cell activation, the so-called extra-follicular activation. This produces fast-reacting antibodies, which seem to bypass many known safety checks. , And has a more accurate immune response.
The extra follicular reaction is very fast, the design time is very short, and it disappears when a more targeted reaction occurs. Between 2015 and 2018, researchers found that these additional follicular immune system responses were common in patients with autoimmune diseases (such as lupus), and they usually showed long-term active extracapsular responses. It can cause the production of high levels of self-targeting antibodies and damage organs such as the lungs, heart, and kidneys. damage. The presence of special types of B cells in the blood produced by the additional follicular reaction may be an important indicator of the severity of diseases such as lupus.
In a recently published research report, researchers found that other follicular B cell characteristics in COVID-19 cases are similar to those of active lupus. In the body's initial response to infection, severely ill patients often experience rapid activation of the antibody production fast track, after which these patients produce high levels of virus-specific antibodies, some of which contain viruses. It can coordinate, but in addition to these protective antibodies, some of the antibodies that researchers have observed are also suspicious, and seem to be an antibody that appears in autoimmune diseases such as lupus. Finally, patients with these autoimmune B-cell responses perform poorly and have an increased incidence of systemic organ failure and death. Researchers pointed out that COVID-19 is not an autoimmune disease. The inflammatory response (such as autoimmunity) discovered by the researchers may only reflect the body's normal response to a viral infection. However, even if this reaction is normal, it is not necessarily dangerous. These long-term extra-follicular cells can exacerbate autoimmune diseases through the production of targeted antibodies and inflammation. Currently, scientists say that in appropriate patients, slowing down the patient's immune response with steroid therapy (or even stronger autoimmune therapy) may be the key to fighting COVID-19 infection. We need to realize that there are weapons of existence, and clinicians and scientists need to build their own treatment methods based on this concept. Even with COVID-19, controlling the body's immune response to the virus is as important as controlling the virus itself.