February 17, 2024
2 minute read
February 17, 2024
2 minute read
SCOTTSDALE, Ariz. — The COVID-19 pandemic will lead to a deeper understanding of the relationship between infectious diseases and autoimmunity, according to speakers at the Basic and Clinical Immunology Symposium for Busy Clinicians. It is said that there is a possibility.
Leonard Calabrese
“The integrated immune response is a balance.” Leonard Calabrese, DO; RJ Fazenmeyer Cleveland Clinic Chair of Clinical Immunology, Medical Editor-in-Chief heliorheumatidaehe told the attendees. “On the one hand, we have effector mechanisms such as cells, cytokines, and chemokines that work together in a kind of way to trigger an inflammatory response that is regulated once it is in effect. It has important tolerogenic and regulatory powers. This is why every time you get a cold, your immune response is not suppressed and you don't develop lymphoma.”
popularization of COVID-19 pandemic has provided researchers with ample opportunity to understand these immune responses.
“The SARS-CoV-2 pathogen is ubiquitous,” Calabrese said. “We're exposed to it over and over again.”
The rheumatology community has long debated the viral hypothesis to explain the pathogenesis of rheumatism. Rheumatism and autoimmune diseases, according to Calabrese. For example, although the link between the Epstein-Barr virus has been established, questions remain.
“EBV and lupus are intriguing areas of research, but they are not explained in a three-dimensional way,” he says.
What is known is that when we come into contact with a pathogen, our innate immune system acts as an “early warning system” and “comes to the forefront,” Calabrese said. However, there are still many unknowns about how the innate immune response transitions to the acquired immune response. The lack of understanding surrounding these reactions is highlighted by the unpredictability of: COVID-19 infection in any particular individual.
“We still don't understand why some people don't get it and others get it,” Calabrese said.
Digging deeper, Calabrese discussed two broad categories of potential triggers of immune responses: pathogen-associated molecular patterns and damage-associated molecular patterns. “This is a good workable paradigm,” he said.
Part of that response/paradigm includes the interferon response observed in SARS-CoV-2 infection and in many rheumatic and autoimmune diseases.
“The focus is on the interferon response. great interest in rheumatology,” he said. “When young, healthy people die from COVID-19, many of them had heterozygous mutations in the type 1 interferon pathway.”
Complicating the situation, Calabrese says, interferon can be “both friend and foe,” depending on the situation. “If interferon stops the coronavirus in our noses, then it's friendly,” he said. “It's very unkind if it's unleashed and unchecked because it can contribute to both the cytokine storm and the development of autoimmunity.”
Researchers are currently studying both the positive and negative effects of interferon in relation to SARS-CoV-2 infection and autoimmunity. It is clear that autoantibodies are produced when a virus occurs. What's not clear, Calabrese said, is whether that will necessarily lead to the development of immune disorders. “This is going to be one of the interesting stories for the next few years,” he said.
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