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10.3389/fphar.2020.569849

http://scihub22266oqcxt.onion/10.3389/fphar.2020.569849
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33424586!7794008!33424586
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suck abstract from ncbi


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pmid33424586      Front+Pharmacol 2020 ; 11 (ä): 569849
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  • Autophagy Modulation in Lymphocytes From COVID-19 Patients: New Therapeutic Target in SARS-COV-2 Infection #MMPMID33424586
  • Vomero M; Barbati C; Colasanti T; Celia AI; Speziali M; Ucci FM; Ciancarella C; Conti F; Alessandri C
  • Front Pharmacol 2020[]; 11 (ä): 569849 PMID33424586show ga
  • Severe Acute Respiratory Syndrome Coronavirus 2 (SARS-CoV-2) is the novel coronavirus, causing coronavirus disease 2019 (COVID-19). During virus infection, several pro-inflammatory cytokines are produced, leading to the "cytokine storm." Among these, interleukin (IL)-6, tumor necrosis factor-alpha (TNF-alpha), and IL-1beta seem to have a central role in the progression and exacerbation of the disease, leading to the recruitment of immune cells to infection sites. Autophagy is an evolutionarily conserved lysosomal degradation pathway involved in different aspects of lymphocytes functionality. The involvement of IL-6, TNF-alpha, and IL-1beta in autophagy modulation has recently been demonstrated. Moreover, preliminary studies showed that SARS-CoV-2 could infect lymphocytes, playing a role in the modulation of autophagy. Several anti-rheumatic drugs, now proposed for the treatment of COVID-19, could modulate autophagy in lymphocytes, highlighting the therapeutic potential of targeting autophagy in SARS-CoV-2 infection.
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