The Role of TLR-2 in Lethal COVID-19 Disease Involving Medullary and Resident Lung Megakaryocyte Up-Regulation in the Microthrombosis Mechanism.
Giuseppe PannoneMaria Carmela PedicilloIlenia Sara De StefanoFrancesco AngelillisRaffaele BarileChiara PannoneGiuliana VillaniFrancesco MieleMaurizio MunicinòAndrea RonchiGaetano ServiddioFederica Zito MarinoRenato FrancoTommaso ColangeloRosanna ZamparesePublished in: Cells (2024)
Microthrombosis in deadly COVID-19+ lung disease is associated with an increase in the number of CD61+ platelets and megakaryocytes in the pulmonary interstitium, as well as their functional activation; this phenomenon is associated with increased expression of innate immunity TLR2+ cells, which binds the SARS-CoV-2 E protein, and significantly with the persistence of the Spike-S1 viral sequence.
Keyphrases
- sars cov
- toll like receptor
- respiratory syndrome coronavirus
- inflammatory response
- induced apoptosis
- immune response
- coronavirus disease
- poor prognosis
- cell cycle arrest
- pulmonary hypertension
- binding protein
- nuclear factor
- patient safety
- quality improvement
- endoplasmic reticulum stress
- oxidative stress
- cell death
- small molecule
- nk cells