Founder’s Corner: Making of the Autoimmunity + COVID-19 Colloquium

Background on the Noel Rose Scientific Colloquium 

For over 23 years, the Autoimmune Association has hosted scientific colloquia, bringing together key researchers from across disciplines to advance the understanding of autoimmune diseases. The colloquia culminated in a published scientific paper to stimulate further research in the scientific community. Over the years, the Colloquia took shape in different forms – from large gatherings of scientific minds to small, invitation only discussions. The Colloquia drew interest from across the healthcare ecosystem and were funded by  NIH grants, corporations, health agencies, foundations, and individual donors. 

In 2013, when the NIH significantly reduced funding for the large-scale meetings, Dr. Noel Rose, a founding member and Chair of the Autoimmune Association’s Scientific Advisory Board, and I reviewed how we could have a more substantial impact with less funding. We determined that smaller one-day colloquiums with specific, forward-thinking topics would best meet our aims. With help from the Scientific Advisory Board, Dr. Rose and I organized one or two of these colloquiums a year, bringing together 16-18 top leaders of autoimmune research to discuss their work and engage in active discussion about new research ideas. The colloquiums were successful and gained a high level of respect from the scientific community. The Autoimmune Association Board of Directors renamed the colloquium the Noel Rose Scientific Colloquium in honor of Dr. Rose’s outstanding work in organizing the colloquia. 

Origins of the COVID-19 and Autoimmunity Colloquium 

Full publication can be viewed here.

Prior to the COVID-19 pandemic, the Autoimmune Association was in the process of collaborating with Dr. Jason Knight and Dr. Joseph McCune from the University of Michigan to organize a colloquium on the role of antiphospholipid antibodies in infection and autoimmune diseases. Antiphospholipid antibodies attack phospholipids, a type of fat in the membrane of our cells, causing cell damage. This cell damage can eventually result in blood clots and thrombosis. However, as we were organizing the colloquium, the COVID-19 outbreak occurred. Following findings that blood clots and thrombosis were linked to severe COVID-19, autoimmune researchers wondered whether antiphospholipid antibodies and autoimmunity could be involved. Therefore, we decided to restructure the colloquium to focus on the role of autoimmunity in COVID-19. 

In May of 2021, scientists from multiple disciplines and specialties came together at the 15th Noel Rose Scientific Colloquium to discuss two important questions: 1) Does pre-existing autoimmunity contribute to severe COVID-19? And 2) can COVID-19 cause autoimmunity? The colloquium resulted in an exciting, collaborative discussion and transfer of ideas. The presenters wrote a scientific article highlighting the outcomes of the conversation to share with the scientific community. The article was published this month in the Journal of Clinical Investigation, a top journal focused on biomedical science and the advancement of medical practice. This blog captures some of the key findings included in the publication. 

Does pre-existing autoimmunity contribute to severe COVID-19? 

The outcomes of COVID-19 are variable, ranging from no symptoms to severe pneumonia and death. Although we know some risk factors for severe COVID-19, such as age and pre-existing medical conditions, some patients develop severe COVID-19 for unknown reasons. Recent work from the laboratory of Dr. Jean-Laurent Casanova at Rockefeller University found that in some patients, severe disease may result from a defective interferon response1. Interferons are crucial proteins in the early antiviral response, as they alert the immune system about viral infection. Dr. Casanova and others demonstrated that approximately 10-15% of patients with severe COVID-19 produce antibodies against interferons. These antibodies prevent interferon function, impairing the early immune response to COVID-19 and contributing to the viral spread. These findings provide important insights into the treatment of these patients. 

Can COVID-19 cause autoimmunity? 

Many features of COVID-19 are similar to autoimmune disease, and a small number of COVID-19 patients have developed different autoimmune diseases, suggesting that COVID-19 may induce autoimmunity in some patients. Other viruses are also linked to autoimmunity and are thought to induce autoimmunity in various ways. As one example, Epstein-Barr virus is thought to contribute to lupus through multiple mechanisms2, including the production of autoantibodies that target proteins or cells of the body. Similarly, important studies3 have found that more than 50% of patients with severe COVID-19 have autoantibodies, including those commonly found in other autoimmune diseases, such as antiphospholipid antibodies. Furthermore, the laboratory of Dr. Ignacio Sanz at Emory University identified high levels of a type of B cell associated with lupus and autoantibodies in the blood of patients with COVID-194. 

Future research 

The presenters at the COVID-19 and Autoimmunity colloquium identified three critical areas for future research. Although studies have identified autoantibodies following COVID-19, it is still unknown how long the autoantibodies will remain in the body or whether they will eventually lead to an autoimmune disease. It will also be important to study whether autoantibodies contribute to the long-term symptoms following COVID-19 in some patients (frequently referred to as Long COVID), as the diverse symptoms and similarities to autoimmune disease suggest autoantibodies may play a role. Finally, research should determine whether treatments and vaccinations alter the production of autoantibodies and autoimmune response following COVID-19. These areas of research  will require large-scale studies that follow patients for an extended period of time. 

Together, the researchers agreed that the COVID-19 pandemic provides a once-in-a-lifetime opportunity to determine how a virus can enhance and trigger autoimmunity. 

References 

1. Bastard P, et al. Autoantibodies against type I IFNs in patients with life-threatening COVID19. Science. 2020;370(6515):eabd4585. 
2. Jog NR, et al. Association of Epstein-Barr virus serological reactivation with transitioning to systemic lupus erythematosus in at-risk individuals. Ann Rheum Dis.  2019;78(9):1235. 
3. Chang SE, et al. New-onset IgG autoantibodies in hospitalized patients with COVID-19. Nat Commun. 2021; 14;12(1):5417. 
4. Woodruff MC, et al. Extrafollicular B cell responses correlate with neutralizing antibodies and morbidity in COVID-19. Nat Immunol. 2020;21(12):1506–1516.