Interleukin-10 down-regulates oxLDL induced expression of scavenger receptor A and Bak-1 in macrophages derived from THP-1 cells

2011 ◽  
Vol 512 (1) ◽  
pp. 30-37 ◽  
Author(s):  
Hong Yang ◽  
Shichao Chen ◽  
Yongqing Tang ◽  
Yalei Dai
2021 ◽  
pp. 174181
Author(s):  
Jianzhen Lei ◽  
Jingheng Ye ◽  
Rong She ◽  
Ruyi Zhang ◽  
Yanan Wang ◽  
...  

2006 ◽  
Vol 53 (2) ◽  
pp. 257-268 ◽  
Author(s):  
Jolanta Zuwała-Jagiełło

Highly efficient systems remove the toxic and proinflammatory haemoglobin from the circulation and local sites of tissue damage. Macrophages are major haemoglobin-clearing cells; CD163 was recently recognized as the specific haemoglobin scavenger receptor (HbSR). It is tightly involved in both physiological as well as pathophysiological processes, such as cytoprotection and inflammation. Haemoglobin functions as a double-edged sword. In moderate quantities and bound to haptoglobin, it forms a ligand for haemoglobin scavenger receptor CD163/HbSR, but when unleashed in large amounts, it can become toxic by mediating oxidative stress and inflammation. CD163/HbSR plays a crucial role in the control of inflammatory processes, probably in part through its effects on both ferritin induction and subsequent induction of antiinflammatory pathways through interleukin-10 and haem oxygenase. Besides the observation that the haemoglobin scavenger receptor provides a promising target for new treatment possibilities, it offers a novel view on the aetiology of diverse physiological as well as pathophysiological processes. In addition, monocyte CD163/HbSR and soluble CD163/HbSR are potential diagnostic tools in a variety of disease states, such as inflammation, atherosclerosis, transplant rejection, and carcinoma.


Biochemistry ◽  
2009 ◽  
Vol 48 (50) ◽  
pp. 11858-11871 ◽  
Author(s):  
Claudine Neyen ◽  
Annette Plüddemann ◽  
Pietro Roversi ◽  
Benjamin Thomas ◽  
Lei Cai ◽  
...  

2009 ◽  
Vol 46 (6) ◽  
pp. 1109-1119 ◽  
Author(s):  
Justyna Rzepecka ◽  
Sebastian Rausch ◽  
Christian Klotz ◽  
Corinna Schnöller ◽  
Tina Kornprobst ◽  
...  

Blood ◽  
2011 ◽  
Vol 117 (4) ◽  
pp. 1319-1328 ◽  
Author(s):  
Subhankar Mukhopadhyay ◽  
Audrey Varin ◽  
Yunying Chen ◽  
Baoying Liu ◽  
Karl Tryggvason ◽  
...  

Abstract Phagocytic and pathogen sensing receptors are responsible for particle uptake and inflammation. It is unclear how these receptors' systems influence each other's function to shape an innate response. The class-A scavenger receptors SR-A (scavenger receptor A) and MARCO (macrophage receptor with collagenous structure) are 2 well-characterized phagocytic receptors that are unable to initiate inflammatory responses by themselves, yet are implicated in the pathogenesis of various inflammatory disorders. However, the mechanism for such an apparent discrepancy is still unclear. We utilized SR-A−/−, MARCO−/−, and SR-A−/−-MARCO−/− mice, along with microbe-derived, environmental, and synthetic polyanions to assess the inflammatory responses following combinatorial ligation of SR-A/MARCO and selected Toll-like receptors (TLRs) and nucleotide-binding oligomerization domain (NOD)–like receptors (NLRs) by their shared ligands. In addition to ligating SR-A and MARCO, these agonists also selectively activated the cell-surface sensor TLR4, endosomal TLR3, and the cytosolic NOD2 and NALP3 (NACHT domain–, leucine-rich repeat–, and pyrin domain–containing protein 3). We show that, following recognition of common ligands, SR-A and MARCO attenuate TLR4-mediated responses while enhancing responses by the intracellular TLR3, NOD2, and NALP3. We conclude that SR-A/MARCO-mediated rapid ligand internalization prevented sensing by surface TLRs while increasing ligand availability in intracellular compartments, thus allowing sensing and robust responses by intracellular sensors.


FEBS Journal ◽  
2019 ◽  
Vol 287 (2) ◽  
pp. 310-324
Author(s):  
Mengying Xie ◽  
Yue Yin ◽  
Liqian Chen ◽  
Aiping Yin ◽  
Yan Liu ◽  
...  

2012 ◽  
Vol 209 (1) ◽  
pp. 109-121 ◽  
Author(s):  
Dapeng Li ◽  
Gabrielle Romain ◽  
Anne-Laure Flamar ◽  
Dorothée Duluc ◽  
Melissa Dullaers ◽  
...  

Dendritic cells (DCs) can initiate and shape host immune responses toward either immunity or tolerance by their effects on antigen-specific CD4+ T cells. DC-asialoglycoprotein receptor (DC-ASGPR), a lectinlike receptor, is a known scavenger receptor. Here, we report that targeting antigens to human DCs via DC-ASGPR, but not lectin-like oxidized-LDL receptor, Dectin-1, or DC-specific ICAM-3–grabbing nonintegrin favors the generation of antigen-specific suppressive CD4+ T cells that produce interleukin 10 (IL-10). These findings apply to both self- and foreign antigens, as well as memory and naive CD4+ T cells. The generation of such IL-10–producing CD4+ T cells requires p38/extracellular signal-regulated kinase phosphorylation and IL-10 induction in DCs. We further demonstrate that immunization of nonhuman primates with antigens fused to anti–DC-ASGPR monoclonal antibody generates antigen-specific CD4+ T cells that produce IL-10 in vivo. This study provides a new strategy for the establishment of antigen-specific IL-10–producing suppressive T cells in vivo by targeting whole protein antigens to DCs via DC-ASGPR.


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