C1q/tumour necrosis factor-related protein-9 aggravates lipopolysaccharide-induced inflammation via promoting NLRP3 inflammasome activation

2022 ◽  
Vol 104 ◽  
pp. 108513
Author(s):  
Dan Xu ◽  
Xin Zhou ◽  
Jiying Chen ◽  
Na Li ◽  
Shiyan Ruan ◽  
...  
Keyword(s):  
Tumour Necrosis Factor ◽  
Nlrp3 Inflammasome ◽  
Tumour Necrosis ◽  
Inflammasome Activation ◽  
Related Protein ◽  
Nlrp3 Inflammasome Activation ◽  
Necrosis Factor

scholarly journals Obesity and chronic kidney disease progression—the role of a new adipocytokine: C1q/tumour necrosis factor-related protein-1

2018 ◽  
Vol 12 (3) ◽  
pp. 420-426 ◽  
Author(s):  
Diego Barbieri ◽  
Marian Goicoechea ◽  
Maria Dolores Sánchez-Niño ◽  
Alberto Ortiz ◽  
Eduardo Verde ◽  
...  
Keyword(s):  
Chronic Kidney Disease ◽  
Kidney Disease ◽  
Disease Progression ◽  
Tumour Necrosis Factor ◽  
Tumour Necrosis ◽  
Related Protein ◽  
Chronic Kidney Disease Progression ◽  
Kidney Disease Progression ◽  
Necrosis Factor

scholarly journals Glucocorticoid-Induced Tumour Necrosis Factor Receptor-Related Protein: A Key Marker of Functional Regulatory T Cells

2015 ◽  
Vol 2015 ◽  
pp. 1-17 ◽  
Author(s):  
Simona Ronchetti ◽  
Erika Ricci ◽  
Maria Grazia Petrillo ◽  
Luigi Cari ◽  
Graziella Migliorati ◽  
...  
Keyword(s):  
T Cells ◽  
Regulatory T Cells ◽  
Tumour Necrosis Factor ◽  
Tumour Necrosis ◽  
Protein A ◽  
Tumour Necrosis Factor Receptor ◽  
Related Protein ◽  
Activated T Cells ◽  
Functional Studies ◽  
Necrosis Factor

Glucocorticoid-induced tumour necrosis factor receptor-related protein (GITR, TNFRSF18, and CD357) is expressed at high levels in activated T cells and regulatory T cells (Tregs). In this review, we present data from mouse and human studies suggesting that GITR is a crucial player in the differentiation of thymic Tregs (tTregs), and expansion of both tTregs and peripheral Tregs (pTregs). The role of GITR in Treg expansion is confirmed by the association of GITR expression with markers of memory T cells. In this context, it is not surprising that GITR appears to be a marker of active Tregs, as suggested by the association of GITR expression with other markers of Treg activation or cytokines with suppressive activity (e.g., IL-10 and TGF-β), the presence of GITR+cells in tissues where Tregs are active (e.g., solid tumours), or functional studies on Tregs. Furthermore, some Treg subsets including Tr1 cells express either low or no classical Treg markers (e.g., FoxP3 and CD25) and do express GITR. Therefore, when evaluating changes in the number of Tregs in human diseases, GITR expression must be evaluated. Moreover, GITR should be considered as a marker for isolating Tregs.

C1q-tumour necrosis factor-related protein-3 exacerbates cardiac hypertrophy in mice

2018 ◽  
Vol 115 (6) ◽  
pp. 1067-1077 ◽  
Author(s):  
Zhen-Guo Ma ◽  
Yu-Pei Yuan ◽  
Xin Zhang ◽  
Si-Chi Xu ◽  
Chun-Yan Kong ◽  
...  
Keyword(s):  
Cardiac Hypertrophy ◽  
Tumour Necrosis Factor ◽  
Tumour Necrosis ◽  
Related Protein ◽  
Necrosis Factor

scholarly journals THE COMPLEMENT C1Q TUMOUR NECROSIS FACTOR-RELATED PROTEIN 1 LEVEL IN PATIENTS WITH SLEEP APNOEA AND PRIMARY ALDOSTERONISM

Heart ◽  
2012 ◽  
Vol 98 (Suppl 2) ◽  
pp. E102.1-E102
Author(s):  
Yao Xiao-guang ◽  
Cheng Wei-ping ◽  
Ma Wan-yong ◽  
Yan Zhi-tao ◽  
Bi Yun-wei ◽  
...  
Keyword(s):  
Tumour Necrosis Factor ◽  
Primary Aldosteronism ◽  
Tumour Necrosis ◽  
Sleep Apnoea ◽  
Related Protein ◽  
Complement C1q ◽  
Necrosis Factor

Anti-Inflammatory Activity of Lobaric Acid via Suppressing NF-κB/MAPK Pathways or NLRP3 Inflammasome Activation

Planta Medica ◽  
2018 ◽  
Vol 85 (04) ◽  
pp. 302-311 ◽  
Author(s):  
Hee-Weon Lee ◽  
JinWook Kim ◽  
Joung-Han Yim ◽  
Hong-Kum Lee ◽  
Suhkneung Pyo
Keyword(s):  
Nlrp3 Inflammasome ◽  
Inflammatory Responses ◽  
Inflammatory Diseases ◽  
Biological Activities ◽  
Inflammasome Activation ◽  
Mapk Pathways ◽  
Nlrp3 Inflammasome Activation ◽  
Mitogen Activated Protein ◽  
Factor Α ◽  
Necrosis Factor

Lobaric acid (LA) is a constituent of the lichen Stereocaulon alpinum. LA has multiple biological activities, including antibacterial and antioxidant ones. The purpose of this study was to investigate the effect of LA and its mechanism on lipopolysaccharide (LPS)-induced inflammatory responses in macrophages. Macrophages were pretreated with different concentrations of LA (0.2 – 20 µM), followed by LPS stimulation. LA treatment of LPS stimulated macrophages decreased their nitric oxide production and the expression of cyclooxygenase-2 and prostaglandin E2. LA also significantly reduced the production of tumor necrosis factor-α and interleukin (IL)-6 by inhibiting the activation of mitogen-activated protein kinases (MAPKs) and nuclear factor-kappa B (NF-κB). Additionally, LA inhibited the production of IL-1β and IL-18, as well as caspase-1 maturation, by inhibition of NLRP3 inflammasome activation in LPS/ATP-stimulated cells. These results strongly suggest that LA could inhibit inflammation by downregulating NF-κB/MAPK pathways and NLRP3 inflammasome activation in activated macrophages. These results reveal a new therapeutic approach to modulate inflammatory diseases linked to deregulated inflammasome activities.

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