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We read with great interest the recent article by Laurent et al.1 which confirmed the potential role of innate lymphoid cells-2 (ILC2) in the establishment of fibrosis in human systemic sclerosis. It provided a novel idea that transforming growth factor-β (TGFβ) downregulates KLRG1 expression on ILC2 and contributes to its low interleukin 10 (IL10) production capacity, finally resulting in skin fibrosis. However, we feel confused when reading some parts of the article.
From the design of the overall experiment, we can clearly understand that the authors first determined the importance of ILC2 in fibrotic tissues, and then sought out the reason: the low IL10 production caused by TGF-β stimulation. Finally, they conducted relevent cell and animal experiments and draw the final conclusion. However, from the conclusion of the article, it is the reduction of IL10 that leads to the progression of fibrosis? It makes us confused because ILC2 is not the main cell producing IL10. As we all known, IL10 is a cytokine of multi-cell origin and almost all immune cells can synthesize IL102. Meanwhile, despite its relative increase in fibrotic tissues, the numberof Innate lymphoid cells is very rare3. With the diversification of IL10 sources, is the low IL10 production capacity of ILC2 the main cause of fibrosis?
In summary, we respect the original insight and contributions of the authors, and believe an in-depth study of the role of IL10 may be a new research direction.
1. Laurent P, Allard B, Manicki P, et al. TGFβ promotes low IL10-producing ILC2 with profibrotic ability involved in skin fibrosis in systemic sclerosis. Ann Rheum Dis 2021.
2. Saraiva M, O'Garra A. The regulation of IL-10 production by immune cells. Nat Rev Immunol 2010;10:170-81.
3. Constantinides MG, McDonald BD, Verhoef PA, Bendelac A. A committed precursor to innate lymphoid cells. Nature 2014;508:397-401.