The autoimmune antibodies that occur during infection cause immune cells to clog blood vessels.
One of the serious complications of COVID-19 coronavirus infection is multiple blood clots in the pulmonary blood vessels. Blood clots can be caused by antibodies against our own cells, or autoimmune antibodies that appear with COVID-19. But a thrombus is quite complicated, and antibodies by themselves cannot form a thrombus.
Researchers from the University of Michigan suggested that immune cells, neutrophils, play an important role in “covid” thrombus formation. The autoimmune antibodies that appear in viral inflammation target phospholipid molecules in cell membranes. Phospholipids are also found in the membranes of neutrophils, which serve as the first line of defense against infections. Among the various immune weapons in the arsenal of neutrophils are the so-called DNA networks. ABOUT neutrophil DNA networks we have already told you: a self-destruction program is activated in neutrophils, forcing them to release their own DNA outward. In the resulting network, bacteria, diseased cells become entangled, and if everything happens in a blood vessel, then platelets; and platelets, as you know, are the most important component of the blood coagulation reaction.
Actually, not so long ago we talked about the fact that neutrophilic networks may aggravate the severity of coronavirus infection. Now researchers have suggested that it is autoimmune antibodies that, sitting on neutrophils, activate their self-destruction with the formation of DNA networks. The article in Science Translational Medicine it is said that when such antibodies, taken from patients with COVID-19, were added to neutrophils grown in the laboratory, the neutrophils threw out DNA networks. And when the same antibodies were injected into mice, the mice developed multiple blood clots. In patients with coronavirus, not only the level of autoimmune antibodies increases, but also the level of neutrophils, so that “covid” blood clots can indeed form by this very mechanism.
However, this mechanism is not necessarily the only one. Autoimmune antibodies appear in many patients with COVID-19 and blood clots, but not all. On the other hand, blood clots generally accompany severe inflammation. There are obviously other molecules that are involved in the inflammatory response and that stimulate blood clots.
Autoimmune antibodies against membrane phospholipids occur not only in COVID-19, but also in other infections, both viral and bacterial. In fact, there may even be some benefit from them, because they stimulate the formation of neutrophilic DNA networks and thereby limit the spread of infection in tissues. But if these antibodies begin to provoke blood clots in the blood vessels, the situation can become simply dangerous – in the case of COVID-19, the lungs can simply fail due to multiple blood clots. Why the virus provokes the immune system to synthesize such antibodies remains to be seen; in the meantime, you can think about how to purposefully cleanse the patient’s blood from dangerous antibodies, or at least weaken their thrombus-forming effect.
Based on materials ScienceNews.