T Cell Dynamics in COVID-19, Long COVID and Successful Recovery
🔥Long COVID involves a complex and PERSISTENT IMMUNE DYSREGULATION. #LeonardiEffect
Interesting Russian study:
➡️"While most clinical studies of COVID-19 immunity focus on major T-cell populations, this study represents the comprehensive immune profiling of COVID-19 patients not only in the acute stage of the disease, but also across mid-convalescence (1–3 months since the infection) and long COVID phases."
➡️"Our findings reveal significant alterations in T-cell subsets, particularly in helper (Th) and cytotoxic (CTL) populations, which persist beyond the acute phase of infection and may contribute to the pathogenesis of LC."
➡️"Acute COVID-19 patients exhibited a certain defect in naïve Th cells and an increase in CM Th cells, a pattern that persisted in convalescents but normalized in LC patients."
➡️"This suggests that while Th cell homeostasis may eventually stabilize, the prolonged dysregulation during recovery could play a role in persistent symptoms."
➡️"LC patients displayed elevated Th1 and Th2 responses alongside reduced Tfh cells, indicating potential disruptions in antibodies formation and germinal center function."
➡️"These imbalances may contribute to chronic inflammation and autoantibody production, which are hallmarks of LC."
➡️"Acute infection was marked by an expansion of CM CTLs, while LC patients showed elevated naïve and TEMRA CTLs with reduced effector memory (EM) subsets."
➡️"This shift suggests either impaired viral clearance or ongoing immune dysregulation, possibly driven by persistent antigen exposure or tissue migration of effector cells.
➡️"The positive correlation between TREC levels and naïve T-cell frequencies in LC patients points to residual thymic activity, possibly compensating for peripheral losses during acute infection."
➡️"The observed Th2/Th17 bias supports the hypothesis that LC involves autoimmune mechanisms, potentially driven by molecular mimicry or loss of immune tolerance."
➡️"Our findings underscore the complexity of immune dysregulation in LC, highlighting the potential need for targeted therapeutic strategies."
Conclusion(Layman): Long COVID involves a complex and persistent immune dysregulation, particularly in T-cell subsets, potentially driving chronic inflammation and autoimmunity.
mdpi.com/1422-0067/26/1…
🔥Long COVID involves a complex and PERSISTENT IMMUNE DYSREGULATION. #LeonardiEffect
Interesting Russian study:
➡️"While most clinical studies of COVID-19 immunity focus on major T-cell populations, this study represents the comprehensive immune profiling of COVID-19 patients not only in the acute stage of the disease, but also across mid-convalescence (1–3 months since the infection) and long COVID phases."
➡️"Our findings reveal significant alterations in T-cell subsets, particularly in helper (Th) and cytotoxic (CTL) populations, which persist beyond the acute phase of infection and may contribute to the pathogenesis of LC."
➡️"Acute COVID-19 patients exhibited a certain defect in naïve Th cells and an increase in CM Th cells, a pattern that persisted in convalescents but normalized in LC patients."
➡️"This suggests that while Th cell homeostasis may eventually stabilize, the prolonged dysregulation during recovery could play a role in persistent symptoms."
➡️"LC patients displayed elevated Th1 and Th2 responses alongside reduced Tfh cells, indicating potential disruptions in antibodies formation and germinal center function."
➡️"These imbalances may contribute to chronic inflammation and autoantibody production, which are hallmarks of LC."
➡️"Acute infection was marked by an expansion of CM CTLs, while LC patients showed elevated naïve and TEMRA CTLs with reduced effector memory (EM) subsets."
➡️"This shift suggests either impaired viral clearance or ongoing immune dysregulation, possibly driven by persistent antigen exposure or tissue migration of effector cells.
➡️"The positive correlation between TREC levels and naïve T-cell frequencies in LC patients points to residual thymic activity, possibly compensating for peripheral losses during acute infection."
➡️"The observed Th2/Th17 bias supports the hypothesis that LC involves autoimmune mechanisms, potentially driven by molecular mimicry or loss of immune tolerance."
➡️"Our findings underscore the complexity of immune dysregulation in LC, highlighting the potential need for targeted therapeutic strategies."
Conclusion(Layman): Long COVID involves a complex and persistent immune dysregulation, particularly in T-cell subsets, potentially driving chronic inflammation and autoimmunity.
mdpi.com/1422-0067/26/1…
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