Apr 14, 2020 · Signaling through IGF receptor (IGF1R) activated the protein kinase B-mammalian target of rapamycin (AKT-mTOR) pathway, increased aerobic glycolysis, favored Th17 cell differentiation over that of Treg cells, and promoted a heightened pro-inflammatory gene expression signature.

Signaling through IGF receptor (IGF1R) activated the protein kinase B-mammalian target of rapamycin (AKT-mTOR) pathway, increased aerobic glycolysis, favored Th17 cell differentiation over that of Treg cells, and promoted a heightened pro-inflammatory gene expression signature.

Apr 11, 2008 · The characterization of the new lineage of IL-17-producing CD4+ T helper (Th17) cells has revolutionized our current understanding of T cell-mediated immunity. Over the past five years, there have been many twists and turns as the pathways that lead to Th17 cell differentiation have been elucidated.

These cytokines induce neutrophil production by regulating the expression of granulocyte-colony-stimulating factor (G-CSF) and local recruitment by regulating tissue expression of CXCR2 ligands such as IL-8 1.

Th17 cells are characterized by production of interleukin (IL)-17A (referred to simply as IL-17), IL-17F (closely related and highly homologous to IL-17A), IL-21 and IL-22. In CIA, serum IL-17 levels increase shortly after immunization, and IL-17 mRNA is up-regulated in the synovium after the onset of arthritis .

Nov 1, 2022 · In present study, we studied the regulatory effect of IGFBP5 on T cell immune response in vitro, and the maintenance of Th17/Treg balance in vivo by using dextran sulfate sodium salt (DSS)-induced colitis in mice.

May 1, 2015 · Exogenous Igfs promote Th17 and suppress Treg differentiation in-vitro, yet fail to influence Th1 or Th2 differentiation. Deletion of Igf1R leads to a defect in Stat3 phosphorylation and IL17a production, and enhanced Treg differentiation in-vitro.

Jan 10, 2025 · Exogenous Th17 cells upregulate TGF-β to promote the upregulation of the surface marker molecule Foxp 3 in Treg cells and inhibit the expression of IL-23R in Th17 cells, thereby causing damage to Th17 cells.

Feb 11, 2013 · Combination of TGF-β1 and IL-6 is sufficient to induce Th17 differentiation from naïve CD4 + T cells, but IL-23 produced by the activated innate cells is critical for stabilizing Th17 cells and for acquiring pathogenic functions. 1, 4 Also results from experimental autoimmune encephalomyelitis (EAE) in T-bet-deficient mice demonstrated that ence...

Our results indicate that IGF signaling promotes the differentiation of Th17 cells while simultaneously suppressing development of Treg cells and modulates development of immune-mediated inflammation in experimental autoimmune encephalomyelitis (EAE).