PMC:7546716 / 5392-6466 JSONTXT

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{"target":"https://pubannotation.org/docs/sourcedb/PMC/sourceid/7546716","sourcedb":"PMC","sourceid":"7546716","source_url":"https://www.ncbi.nlm.nih.gov/pmc/7546716","text":"The dysregulation of GATA3+ Foxp3+ Treg cells might result in impaired immunological tolerance and increased secretion of type 2 cytokines, thus promoting autoinflammatory lung disease.16 TGFβ2, which is also increased in the bronchoalveolar lavage fluid of patients with COVID-19,11 might further enhance ST2 expression in innate lymphoid cells, and IL-33 is the key cytokine that drives these cells to differentiate into type 2 innate lymphoid cells (ILC2).17 ILC2 subsequently elicit lung inflammation by releasing large amounts of IL-9, which promotes their own survival and expands γδ T cells.18, 19 IL-9 is known to stimulate proliferation and expansion of Vγ9Vδ2+ T cells that have a predominantly effector memory phenotype and a combined Th1–Th17 cytokine response profile.19 When exposed to TGFβ, γδ T cells can also become an important source of IL-9.20 By acting in both autocrine and paracrine manners, IL-33-induced IL-9 might sustain a proinflammatory ILC2–γδT cell axis in the lungs of patients with COVID-19, thus initiating mild–moderate forms of 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