ArticleThe Journal of clinical investigation2023
CTRP4/interleukin-6 receptor signaling ameliorates autoimmune encephalomyelitis by suppressing Th17 cell differentiation.
Article in The Journal of clinical investigation, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed, 12 citations in OpenAlex.
- TAB2 Causes Neuronal Damage by Aggravating Microglia-Mediated Neuroinflammation in Parkinson's Disease.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Decreased adipokine CTRP4 in CAD patients: CTRP4 attenuates atherosclerosis via inhibition of RAGE and TLR4.Clinical and translational medicine · 2026Article
- CD4European journal of immunology · 2026Article
- C1q/TNF-Related Protein 4 (C1QTNF4) Acts as an Adipokine That Ameliorates Diet-Induced Obesity by Improving Energy Metabolism and Alleviating Adipose Inflammation.Mediators of inflammation · 2026Article
- Imiquimod promotes Th1 and Th17 responses via NF-κB-driven IL-12 and IL-6 production in anExperimental and therapeutic medicine · 2025Article
- Febrile temperature-regulated TRPV1 in CD4Journal of neuroinflammation · 2025Article
- Article
- The immunoregulatory role of helper T cells inFrontiers in immunology · 2025Review
- TGR5 deficiency in excitatory neurons ameliorates Alzheimer's pathology by regulating APP processing.Science advances · 2024Article
- Article
- Association of serum CTRP4 levels with vascular endothelial function in patients with type 2 diabetes mellitus: CTRP4 ameliorating inflammation, proliferation and migration in human umbilical vein endothelial cells.Acta diabetologica · 2024Article
- Unveiling the role of interleukin-6 in pancreatic cancer occurrence and progression.Frontiers in endocrinology · 2024Review
Corrections and comments
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Authors and funding
10 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
C1q/TNF-related protein 4 (CTRP4) is generally thought to be released extracellularly and plays a critical role in energy metabolism and protecting against sepsis. However, its physiological functions in autoimmune diseases have not been thoroughly explored. In this study, we demonstrate that Th17 cell-associated experimental autoimmune encephalomyelitis was greatly exacerbated in Ctrp4-/- mice compared with WT mice due to increased Th17 cell infiltration. The absence of Ctrp4 promoted the differentiation of naive CD4+ T cells into Th17 cells in vitro. Mechanistically, CTRP4 interfered with the interaction between IL-6 and the IL-6 receptor (IL-6R) by directly competing to bind with IL-6R, leading to suppression of IL-6-induced activation of the STAT3 pathway. Furthermore, the administration of recombinant CTRP4 protein ameliorated disease symptoms. In conclusion, our results indicate that CTRP4, as an endogenous regulator of the IL-6 receptor-signaling pathway, may be a potential therapeutic intervention for Th17-driven autoimmune diseases.
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