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University of Michigan team links ‘rogue’ antibodies to COVID blood clots

blood clot
Misbehaving antibodies that attack the body’s own blood vessel cells may play a role in COVID by making blood vessels “sticky” and susceptible to blood clots, University of Michigan researchers concluded. (University of Michigan illustration.)

“Rogue” antibodies that attack the lining of blood vessels may contribute to deadly blood-clotting in some COVID-19 patients, according to a new study by University of Michigan researchers. 

The study, published Thursday in  the peer-reviewed journal Arthritis & Rheumatology, is early research. But it could become foundational science to future treatments as it becomes ever more clear COVID-19 will circulate for years, said Dr. Jason Knight, a rheumatologist at Michigan Medicine and co-author of the study.


Using blood and serum from 244 patients hospitalized with COVID,  researchers found higher-than-expected levels of “antiphospholipid autoantibodies” in about half of the patients — a type of antibody some call “rogue.”


Why rogue? 

While antibodies are Y-shaped proteins that help the body neutralize infections, autoantibodies are different. They mistakenly target and sometimes damage the body’s own systems and organs. In patients with autoimmune disorders, such as lupus and antiphospholipid syndrome, they can trigger blood clots in the arteries and veins.

As COVID-19 first raged across the globe in 2020, the U-M team and researchers from the National Institutes of Health found autoantibodies in COVID patients. They learned the autoantibodies caused “a striking amount of clotting” in lab mice injected with them. 

Dr. Jason Knight
The early research on blood vessel cells could one day lead to new COVID treatments, said University of Michigan researcher Dr. Jason Knight. (Courtesy photo)

They and other scientists suspected they played a pivotal role in COVID’s potentially deadly cascade of symptoms — specifically related to blood clots in COVID patients. Clotting may account for roughly 1-in-5 COVID-19 deaths, NIH researchers concluded in a separate paper published in September.

Now, the U-M team may have found clues to learn precisely why.

In the lab, the autoantibodies unexpectedly recognized and then bound to endothelial cells, which line the blood vessels and release enzymes that help control blood clotting and keep blood flowing through the body.

Consider accidentally cutting your finger while chopping vegetables. In that case, clotting is normal and beneficial since it keeps you from bleeding out.

But in COVID patients, the autoantibodies activated endothelial cells, causing them to become “sticky,” and attracting other cells to the wall lining, causing blood clots.  

“They turn on programs they might use in an injury, and they become much stickier,” Knight said of the autoantibodies. “Now, the cells in our blood — instead of just flowing by the endothelial cells nicely, like in normal times — will start to stick to that wall, and that’s the beginning of a blood clot.”

Those clots can block vessels, triggering strokes, causing long-term damage to organs and — especially in COVID — lung problems that impair patients’ ability to breathe.


When researchers removed antiphospholipid autoantibodies from COVID blood samples, the overactivated clotting processes disappeared.

More research is needed, but the U-M study may lead to screening and treatment for COVID patients at greatest risk of blood clots — both during an the initial infection when the immune system first goes haywire, or later, among those who suffer from a constellation of lingering symptoms known as long COVID.

“We're gonna have to individualize” treatment for long COVID patients, Knight said. “There's not gonna be a long COVID pill that is universally successful.”

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