ArticleDiabetologia2008
Suppressor of cytokine signalling-3 expression inhibits cytokine-mediated destruction of primary mouse and rat pancreatic islets and delays allograft rejection.
Article in Diabetologia, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed, 39 citations in OpenAlex.
- A surviving beta cell subpopulation enriched in patients with T1D.bioRxiv : the preprint server for biology · 2026Article
- New insight into the role of SOCS family in immune regulation and autoimmune pathogenesis.Journal of advanced research · 2026Review
- SOCS3 inhibits the mesenchymal stromal cell secretory factor SDF-1-mediated improvement of islet function in non-obese diabetic mice.Stem cell research & therapy · 2023Article
- Cavin-1 promotes M2 macrophages/microglia polarization via SOCS3.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2022Article
- SOCS3 overexpression in T cells ameliorates chronic airway obstruction in a murine heterotopic tracheal transplantation model.Surgery today · 2019Article
- Suppressors of Cytokine Signaling in Sickness and in Health of Pancreatic β-Cells.Frontiers in immunology · 2016Review
- The efficacy of SPA0355 in protecting β cells in isolated pancreatic islets and in a murine experimental model of type 1 diabetes.Experimental & molecular medicine · 2013Article
- Ciliary neurotrophic factor protects mice against streptozotocin-induced type 1 diabetes through SOCS3: the role of STAT1/STAT3 ratio in β-cell death.The Journal of biological chemistry · 2012Article
- The immunosuppressive role of adenosine A2A receptors in ischemia reperfusion injury and islet transplantation.Current diabetes reviews · 2012Article
- SOCS3 deficiency promotes M1 macrophage polarization and inflammation.Journal of immunology (Baltimore, Md. : 1950) · 2012Article
- Ciliary neurotrophic factor (CNTF) protects non-obese Swiss mice against type 2 diabetes by increasing beta cell mass and reducing insulin clearance.Diabetologia · 2012Article
- Impaired miR-146a expression links subclinical inflammation and insulin resistance in Type 2 diabetes.Molecular and cellular biochemistry · 2011Article
- Current status of immunomodulatory and cellular therapies in preclinical and clinical islet transplantation.Journal of transplantation · 2011Article
- Molecular mechanistic associations of human diseases.BMC systems biology · 2010Article
- SOCS3-mediated blockade of JAK/STAT3 signaling pathway reveals its major contribution to spinal cord neuroinflammation and mechanical allodynia after peripheral nerve injury.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2010Article
- Constitutive expression of suppressor of cytokine signalling-3 in skeletal muscle leads to reduced mobility and overweight in mice.Diabetologia · 2009Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
10 authors at 4 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
aims/hypothesisThe pro-inflammatory cytokines IL-1 and IFNgamma are critical molecules in immune-mediated beta cell destruction leading to type 1 diabetes mellitus. Suppressor of cytokine signalling (SOCS)-3 inhibits the cytokine-mediated destruction of insulinoma-1 cells. Here we investigate the effect of SOCS3 in primary rodent beta cells and diabetic animal models.
methodsUsing mice with beta cell-specific Socs3 expression and a Socs3-encoding adenovirus construct, we characterised the protective effect of SOCS3 in mouse and rat islets subjected to cytokine stimulation. In transplantation studies of NOD mice and alloxan-treated mice the survival of Socs3 transgenic islets was investigated.
resultsSocs3 transgenic islets showed significant resistance to cytokine-induced apoptosis and impaired insulin release. Neither glucose-stimulated insulin release, insulin content or glucose oxidation were affected by SOCS3. Rat islet cultures transduced with Socs3-adenovirus displayed reduced cytokine-induced nitric oxide and apoptosis associated with inhibition of the IL-1-induced nuclear factor-kappaB and mitogen-activated protein kinase (MAPK) pathways. Transplanted Socs3 transgenic islets were not protected in diabetic NOD mice, but showed a prolonged graft survival when transplanted into diabetic allogenic BALB/c mice. CONCLUSIONS/
interpretationSOCS3 inhibits IL-1-induced signalling through the nuclear factor-kappaB and MAPK pathways and apoptosis induced by cytokines in primary beta cells. Moreover, Socs3 transgenic islets are protected in an allogenic transplantation model. SOCS3 may represent a target for pharmacological or genetic engineering in islet transplantation for treatment of type 1 diabetes mellitus.
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