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Description

however, under strong anti-CD3 stimulation favoring Th1/Th17 polarization, this induction is attenuated (93)

Its mechanism lies in impeding the interaction between TNF- and its receptors

Pulmonary fibrosis (PF) and chronic obstructive pulmonary disease (COPD) (Phase ), further induce endoplasmic reticulum stress and DNA damage, leading to cellular mutations that increase the risk of cancer and promote lung cancer (Phase )