March 1, 2023
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March 1, 2023
Read in 3 minutes
Calabrese L. Advances in Immunology for Non-Immunologists: The Human Immune Response at 30,000 Feet – History as a Model and COVID-19. Presented at Basic and Clinical Immunology for the Busy Clinician February 25-26, 2023. Scottsdale, Arizona (hybrid conference).
Disclosure: Calabrese has consulted or reported for AbbVie, ChemoCentryx, Galvani, Genentech, Gilead Sciences, GlaxoSmithKline, Janssen, Novartis, Sanofi-Regeneron, and UCB.
SCOTTSDALE, Ariz. — COVID-19 research may improve our understanding of immunology by demonstrating that the immune system is “highly alive,” said the Busy Clinician Symposium on Fundamentals and Clinical Research. An immunology speaker said.
“The whole job of the immune system is to protect the body from danger, but not to harm us.” Leonard Calabrese, DO, RJ Fasenmyer, Chair of Clinical Immunology at the Cleveland Clinic and Chief Medical Editor of Healio Rheumatology, told attendees at the hybrid meeting. “He intends to use COVID-19 as a model for how this works in practice.”
First, Calabrese Pathogenesis of COVID-19 infectionfrom the initial innate immune response to acquisition and viral propagation.
“Within five to seven days, adaptive immunity sets in,” he said. “Within 10 days, all the antibodies are formed.”
Calabrese added that while most people have a CD4 response, most people have a CD8 response.
At this point, most patients improve. However, people who progress to the third stage of infection may require hospitalization or die due to high levels. immune inflammatory response.
According to Calabrese, this intersection in understanding the immune system and the emergence of COVID-19 could advance our knowledge of immunology.
“Stage 3 is a very important and enigmatic educational phase of the disease,” he said.
With regard to the myriad of known immune response triggers, Calabrese looked not only at infections, but also foreign antigens and other dangers to the body.
“It’s a lot more sophisticated than we believed,” he said of the immune system.
In particular, the definition of what might be considered “dangerous” to the body has evolved, says Calabrese.
“These hazards could be in very different forms than we knew them 10 or 20 years ago,” he said. “Our immune system can be triggered by what we call neuropsychoimmunological triggers.”
Leonard Calabrese
Atmospheric change, along with climate change, social determinants of health, and exposure to pollution, can cause this.
“Our brain is intimately tied to our immune system,” said Calabrese. “There is a two-way pathway between the brain and the immune system.”
All of this is relevant to COVID-19, Calabrese said, because in addition to the virus itself, the disruption and stress of the pandemic can trigger specific immune responses that can exacerbate viral infections.
These effects may work in tandem with the immunological effects of viruses suggesting a major role in the immune response. For example, when a virus enters a cell, “several he engages Toll-like receptors (TLRs), particularly receptors that recognize RNA,” Calabrese said.
The virus then disrupts immune system homeostasis and activates the inflammasome. While interleukin-1 is involved, proteins respond to other her TLRs, including her TLR-3.
“All of these things can cause an interferon response and inflammation,” says Calabrese. “The choreography of inflammation is very important to how we exist.”
COVID-19 could disrupt that choreography. The amount of research on SARS-CoV-2 is overwhelming, but Calabrese says that understanding interferon’s role in autoantibody production is important for understanding not only the pathogenesis of the virus, but the pathogenesis of the immune response. suggested that it could be an important clue for For any infection or assault.
“Is interferon driving severe COVID?” He said. “Are they just passengers in the car? We don’t know yet.”
However, there are some certainties that may serve as building blocks to answer these questions.
“An interferon acting as an antiviral agent is on your side,” Calabrese said. “When you’re inflamed, you’re the enemy.”
At that point, he offered tips for managing patients infected with the virus.
“You want to build up your defenses early on and use anti-inflammatory drugs later,” Calabrese said. “COVID shows that the immune system is very much alive.”
He added that increased attention to the immune system would benefit the medical and scientific community as a whole.
“A few years ago, if I went to a cocktail party and said I worked in immunology, no one cared,” says Calabrese. “Everybody is an immunologist now.”
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