Abstract
Post-Covid pulmonary fibrosis is evident following severe COVID-19. There is an urgent need to identify the cellular and pathophysiological characteristics of chronic lung squeals of Covid-19 for the development of future preventive and/or therapeutic interventions. Tissue-resident memory T (T(RM)) cells can mediate local immune protection against infections and cancer. Less beneficially, lung T(RM) cells cause chronic airway inflammation and fibrosis by stimulating pathologic inflammation. The effects of Janus kinase (JAK), an inducer pathway of cytokine storm, inhibition on acute Covid-19 cases have been previously evaluated. Here, we propose that Tofacitinib by targeting the CD8(+) T(RM) cells could be a potential candidate for the treatment of chronic lung diseases induced by acute SARS-CoV-2 infection.