2023-09-04 17:46:47
Friendly fire triggered by an accidentally disengaged ‘brake’. This is how – thanks to the encounter with Sars-CoV-2 – some immune cells, among the thousands that circulate in our body, find themselves attacking not an external enemy, but the body. They are cells that are part of our defense system and are able to recognize our organs and tissues and potentially even attack them. However, there is a ‘tolerance program’ which, if active, prevents this ‘self-aggression’ from happening. A study conducted by Humanitas researchers, involving patients with cardiac sequelae from Covid, has shown that the encounter of some of these immune cells with Sars-CoV-2 is able to accidentally turn off the tolerance program, unleashing the cells against heart tissue.
This identified autoimmune mechanism can persist for months after the end of the infection and could also explain other symptoms typically associated with Long Covid. The results of the study are published in the journal Circulation and pave the way for a better understanding of the post virus syndrome. The research stems from the joint work between the group of Marinos Kallikourdis, head of the Adaptive Immunity Laboratory, and the group of Gianluigi Condorelli, director of the Cardiovascular Department of Humanitas, with the support of the team of Marco Francone, head of cardiovascular imaging. All three are professors at Humanitas University. The study was conducted on blood samples of patients hospitalized for Covid in the Irccs Istituto Clinico Humanitas, and was also possible thanks to the support of the Ministry of University and Research and the Umberto Veronesi Ets Foundation.
“Cardiovascular complications are frequent in patients recovered from Covid, especially in those who have suffered from a severe form of the infection – explains Condorelli – Studies tell us that half of patients hospitalized for Covid with high levels of troponin (an indicator of damage to cardiac tissue) have cardiac magnetic resonance abnormalities even 6 months after recovery”. In general, the damage suffered by organs and tissues following an infection such as Covid can be explained by two phenomena, which can coexist: direct aggression by the virus and collateral damage due to the immune response triggered by the virus and then facing incorrectly against the fabric. “The second phenomenon is able to explain the damage to tissues that Sars-CoV-2 did not attack directly – continues Condorelli – In addition to telling us why this damage persists even after infection, i.e. when the virus is no longer present, as happens in Long Covid”.
To understand what happens in the case of cardiovascular complications, the researchers involved patients hospitalized at Humanitas, focusing in particular on those who, 6 months after discharge, still showed heart damage on magnetic resonance imaging. These are people who had no history of cardiovascular disease behind them. “By analyzing the samples of these patients we discovered an abnormal activation of some types of white blood cells – the B cells, those responsible for producing antibodies – and we identified the presence of some auto-antibodies that recognize the tissues of the heart”, they explain the researchers Marco Cremonesi and Arianna Felicetta, first authors of the study on ‘Circulation’.
“As we later demonstrated in a laboratory study, these auto-antibodies are absent in patients hospitalized with Covid but without heart damage and are sufficient to trigger an autoimmune reaction against the heart,” they highlight. “The study data, albeit indicative and derived from a small number of patients, support our starting hypothesis – Kallikourdis intervenes – Heart damage is compatible with a mechanism called ‘loss of immunological tolerance'”. The researchers’ hypothesis is that during the Covid infection some immune cells made to recognize our tissues are accidentally stimulated by the encounter with the virus and turn off ‘the brake’ which, under normal conditions, prevents them from orchestrating an aggression against our body.
“The loss of immunological tolerance could also explain the variety of symptoms of Long Covid: although it is a single mechanism, it can in fact produce very different clinical consequences, depending on the type of specificity of the immune cells that lose tolerance after the accidental encounter with Sars-CoV-2,” continues Kallikourdis. This means that “the same mechanism could explain other autoimmune reactions, for example against nervous tissue, typical of Long Covid”. If further confirmed, the results will help demonstrate the decisive role of immunity in heart disease and the efficacy demonstrated by some immunomodulatory drugs in the treatment of Covid patients.
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