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The multifunctional cytokine transforming growth factor-beta (TGF-β) controls a wide range of biological processes, including embryonic development, adult stem cell differentiation, wound healing, immune regulation, and inflammation. TGF-β family members signal through transmembrane serine/threonine kinase receptors via the canonical SMAD pathway to induce wide-ranging alterations to gene expression and via several non-canonical pathways to regulate the cytoskeleton, cell polarity, and microRNA maturation among other mechanisms. While TGF-β signaling controls the differentiation of mesenchymal stem cells (MSCs) into osteoblasts, chondrocytes, myoblasts, adipocytes, and tenocytes1; the secretion of TGF-β by MSCs also plays a crucial role in the immunomodulatory capacity of MSCs.2 MSCs derived from the umbilical cord or adipose tissue represent a readily available and patient-matched source of immunomodulatory cells that have been assessed at the preclinical and clinical levels in various diseases/disease models; however, we still lack a deep understanding of the mechanisms involved in TGF-β-mediated immunomodulation. In our first Featured Article published this month in STEM CELLS, Park et al. describe the TGF-β-mediated immunomodulatory mechanisms that mediate the alleviation of atopic dermatitis, a chronic allergic skin disorder, following the subcutaneous administration of human umbilical cord blood-derived MSCs (hUCB-MSCs).3 In a Related Article published recently in STEM CELLS Translational Medicine, Noh et al. reported that TGF-β secreted by MSCs polarized microglia, the macrophages of the central nervous system, from a classically-activated phenotype into an inflammation-resolving phenotype to inhibit the neuroinflammatory processes associated with neurodegenerative disorders.4

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