Mar 1, 2016 · In this study, we examined the roles of SOCS family members expressed in M2 macrophages in the regulation of CHS and found that SOCS3 is expressed in M2 macrophages and is involved in the attenuation and/or resolution of …

Suppressors of cytokine signaling (SOCS) have emerged as potential regulators of macrophage function. We have investigated mechanisms of SOCS3 action on type 2 macrophage (M2) differentiation induced by glucocorticoid using human monocytic cell lines and mouse bone marrow-derived macrophages.

Reduction of SOCS3 expression promotes the microglial/macrophage polarization from the M1 to M2 phenotype. The expression profiles of microglial/macrophage phenotypes were evaluated by immunofluorescence staining with Arg1 (A) and iNOS (B) at 7 and 14 days post-ICH.

Jul 28, 2014 · STAT3, STAT6, and PI3K can drive M2 activation and SOCS3 inhibits STAT3 and PI3K. Pathways that trigger SOCS1 in macrophages include STAT1 and NFκB, while SOCS3 expression can be induced by STAT3, NFκB, NOTCH1, PI3K, and MAP kinase activation.

The correlation of SOCS3 expression with several immunosuppressive cells, which can promote T-cell exclusion, were analyzed, including the M2 subtype of tumor-associated macrophages (M2-TAMs), cancer-associated fibroblasts (CAFs), myeloid-derived suppressor cells (MDSCs), and regulatory T (Treg) cells in 40 different cancers based on data ...

Dec 21, 2012 · M1 macrophages are pro-inflammatory, whereas M2 macrophages are involved in tissue repair. Here, Spence et al. study the role of suppressor of cytokine signalling 2 (SOCS2) and SOCS3 in...

Mar 1, 2023 · qPCR, flow cytometry, and western blotting were used to verify the effect of epidermal stem cell-derived exosomes (EpiSC-EXOs) on M2 macrophage polarization and SOCS3 expression. By screening key miRNAs targeting SOCS3 in EpiSC-EXOs by high-throughput sequencing, we verified the mechanism in vitro.

To determine the roles of suppressor of cytokine signaling (SOCS) family members in M2 macrophages in the regulation of CHS, we investigated the expression of SOCS family members in M2 macrophages at the inflammatory sites of CHS.

In M1-activated human monocyte-derived macrophages, SOCS3 silencing, using short interfering RNA technology, resulted in a decreased expression of proinflammatory markers and an increased expression of M2 macrophage markers.

SOCS3 is highly and preferentially expressed in hapten-induced contact hypersensitivity (CHS), which promotes the M2 polarization and participates the attenuation of CHS by suppressing MMP12 production [105].