COVID-19, autoimmunity and rheumatology
As we enter year 2 of the pandemic with some glimmers of hope that we may be seeing the beginning of the end, rheumatology as a field has been heavily engaged in the fight against SARS-CoV-2.
The early phase of the pandemic witnessed a clinical trial landscape with a remarkable array of therapeutic agents in our armamentarium including — but not limited to — glucocorticoids, antimalarials, colchicine, numerous biologics (anti-IL-6, anti-TNF, anti-GMCSF etc.), kinase inhibitors (ie, JAK, BTK and others) and more. Sadly, at the end of the day, aside from glucocorticoids and baricitinib, success stories have been modest.
As a profession, our knowledge and experience have been valued in this struggle and many prominent rheumatologists around the world have been frontline in research and investigation. Where this area of immune therapeutics will go from here is still a work in progress.
More recently, in my opinion, the story has become even more interesting for our profession as our knowledge of immunopathogenesis of COVID-19 has become more granular. Over the past few months, there have been a series of studies documenting the presence of autoreactivity in COVID-19 via detection of strong autoantibody signatures in the course of active disease.
Importantly, there is also evidence that some of these autoantibodies may be functionally important, in particular antiphospholipid antibodies, which are likely participating in immunothrombosis. Much of this important work has come from labs run by rheumatologists including Ignacio Sanz, MD, from Emory University, Jason Knight, MD, PhD, from the University of Michigan, and PJ Utz, MD, from Stanford. These are but a few working on this forefront and I expect to see much more work from our colleagues in the months ahead.
Finally, at the moment one can only wonder what role autoimmunity may be playing in the post-COVID-19 spectrum of illnesses being described. For example, autonomic dysfunction is but one of the syndromes being described in this setting where autoimmune mechanisms have been postulated to be playing a role. While “long COVID” is a work in progress — and now the subject of a $1.15 billion NIH-supported research initiative — it is impossible to say where our field may wind up in the areas of care and research for these patients.
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- Leonard H. Calabrese, DO, is the Chief Medical Editor, Healio Rheumatology, and Professor of Medicine, Cleveland Clinic Lerner College of Medicine of Case Western Reserve University, and RJ Fasenmyer Chair of Clinical Immunology at the Cleveland Clinic.