COVID-19 Antibodies Found to Rewire Immune Cells and Cause Autoimmune Issues Based on Disease Severity
Nikhil Prasad Fact checked by:Thailand Medical News Team Aug 04, 2026 1 hour ago
Severe COVID-19 infections may leave behind far more than protective antibodies. A new study suggests that antibodies produced during severe COVID-19 infections can actively reshape the immune system, promoting inflammatory responses, altering gene regulation, and increasing the likelihood of attacking the body's own proteins. In contrast, antibodies from moderate cases appear to trigger a more balanced immune response that may support tissue repair instead.
New research shows antibodies from severe COVID-19 can reshape immune responses and display broader
autoimmune activity than antibodies from moderate infections
The research was conducted by scientists from Santo Amaro University (UNISA), Brazil, the University of São Paulo Medical School and its Laboratory of Medical Investigation (LIM-56 and LIM-03), Brazil, the Hospital das Clínicas, University of São Paulo, Brazil, and the University Medical Center Groningen, The Netherlands.
COVID-19 Antibodies Do More Than Fight the Virus
Most people think antibodies simply recognize and neutralize viruses. However, the researchers found that antibodies generated after SARS-CoV-2 infection can also directly interact with immune cells, influencing how they behave long after they encounter the virus.
The team purified IgG antibodies from people who had experienced moderate or severe COVID-19 and exposed healthy immune cells to these antibodies in laboratory experiments. This allowed them to study the direct effects of the antibodies without interference from the infection itself. The results showed that antibodies from severe cases behaved very differently from those produced after moderate illness.
Severe COVID-19 Antibodies Push the Immune System Toward Inflammation
One of the most striking findings was that antibodies from severe COVID-19 reduced the number of regulatory T cells, often called Tregs. These specialized immune cells normally help prevent excessive inflammation and stop the immune system from attacking healthy tissues.
The severe COVID-19 antibodies also increased production of interferon-gamma, a powerful inflammatory signaling molecule, in both CD4 and CD8 T cells. At the same time, they reduced several protective signaling molecules, including IL-9, IL-17A, IL-22, and IL-10. Together, these changes created a much more inflammatory immune profile that could potentially contribute to prolonged immune dysfunction.
Moderate COVID-19 Antibodies Produced a Different Response
In contrast, antibodies from people with moderate COVID-19 generated a more balanced pattern. Instead of strongly promoting inflammation, they increased IL-22 production by CD8 T cells.
IL-22 plays an important role in repairing damaged tissues, particularly in the lungs and respiratory tract. This suggests that antibodies generated after milder illness may help support healing while avoiding the excessive inflammatory activity seen after severe disease.
This
Medical News
; report highlights that the quality of antibodies produced after infection may be just as important as the quantity, with disease severity appearing to shape how these antibodies influence the immune system.
Antibodies Also Changed Gene Regulation
The researchers discovered another unexpected effect. The antibodies altered the activity of several microRNAs, tiny molecules that regulate how genes are switched on and off.
Moderate COVID-19 antibodies selectively reduced the activity of nine important microRNAs involved in immune regulation, inflammation, blood vessel function, and cellular survival. Meanwhile, severe COVID-19 antibodies lacked this distinctive regulatory pattern, suggesting that beneficial gene-control mechanisms may be diminished after more serious infections.
Evidence of Broader Autoimmune Activity
Perhaps the most concerning discovery was the difference in autoreactivity. Antibodies from severe COVID-19 recognized a much wider range of human proteins than antibodies from moderate disease.
Many of these targeted proteins are involved in maintaining protein stability and the ubiquitin-proteasome system, which controls protein recycling, stress responses, and immune regulation. The researchers believe this broader autoreactivity could represent an immunological "scar" left behind by severe infection and may help explain why some individuals experience persistent immune disturbances after recovering from COVID-19. Importantly, the antibodies attached to living T cells without causing widespread cell death, indicating they were actively modifying immune function rather than simply damaging cells.
Conclusions
The findings suggest that antibodies produced during COVID-19 are far more biologically active than previously believed. Rather than serving only as virus-fighting molecules, they can directly reshape immune cell behavior, influence inflammatory signaling, regulate gene expression, and recognize the body's own proteins. While the experiments were conducted in laboratory cell cultures and do not prove these effects occur in every patient, they provide compelling evidence that severe COVID-19 generates antibody repertoires with stronger inflammatory and autoimmune characteristics. The researchers say future long-term studies are needed to determine whether these antibody-driven changes contribute to persistent symptoms or autoimmune complications following COVID-19.
The study findings were published in the peer reviewed Journal of Translational Autoimmunity.
https://www.sciencedirect.com/science/article/pii/S2589909026000456
Read Also:
https://www.thailandmedical.news/articles/coronavirus
https://www.thailandmedical.news/articles/long-covid
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