ArticleEuropean journal of immunology2016
Lumican negatively controls the pathogenicity of murine encephalitic TH17 cells.
Article in European journal of immunology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
What it found
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Who cites it
7 citing papers in PubMed, 13 citations in OpenAlex.
- Paracrine regulations of IFN-γ secreting CD4Matrix biology : journal of the International Society for Matrix Biology · 2025Article
- Transcriptomic analysis of a 3D blood-brain barrier model exposed to disturbed fluid flow.Fluids and barriers of the CNS · 2022Article
- Matrix lumican endocytosed by immune cells controls receptor ligand trafficking to promote TLR4 and restrict TLR9 in sepsis.Proceedings of the National Academy of Sciences of the United States of America · 2021Article
- White matter deficits in cocaine use disorder: convergent evidence from in vivo diffusion tensor imaging and ex vivo proteomic analysis.Translational psychiatry · 2021Article
- Communications via the Small Leucine-rich Proteoglycans: Molecular Specificity in Inflammation and Autoimmune Diseases.The journal of histochemistry and cytochemistry : official journal of the Histochemistry Society · 2020Review
- Beneficial roles of probiotics on the modulation of gut microbiota and immune response in pigs.PloS one · 2019Article
- Leptin Promotes Allergic Airway Inflammation through Targeting the Unfolded Protein Response Pathway.Scientific reports · 2018Article
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Authors and funding
9 authors at 3 institutions in 1 country.
Funding
Abstract
TH17 cells play an essential role in the development of both human multiple sclerosis and animal experimental autoimmune encephalomyelitis (EAE). Nevertheless, it is not well understood how the pathogenicity of TH17 cells is controlled in the autoimmune neuroinflammation. In vitro, we found Lumican (Lum), an extracellular matrix (ECM) protein, is selectively expressed by TH17 cells among tested murine TH subsets. Lum deficiency leads to earlier onset and enhanced severity of EAE. This enhanced disease in Lum-deficient mice is associated with increased production of IL-17 and IL-21 and decreased TH17 cell apoptosis. Dysregulation in cytokine production appears to be specific to TH17 cells as TH1 and TH2 cell polarization and/or cytokine production were unaltered. Furthermore, adoptive transfer of myelin oligodendrocyte glycoprotein specific TH17 cells derived from Lum-deficient mice led to earlier onset and increased severity of disease compared to controls highlighting a TH17-cell-intrinsic effect of Lum. Taken together, our results suggest that Lum negatively regulates encephalitic TH17 cells, implicating a potential therapeutic pathway in TH17 cell mediated autoimmune and inflammatory diseases.
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