LC3-associated phagocytosis in myeloid cells, a fireman that restrains inflammation and liver fibrosis, via immunoreceptor inhibitory signaling
| العنوان: | LC3-associated phagocytosis in myeloid cells, a fireman that restrains inflammation and liver fibrosis, via immunoreceptor inhibitory signaling |
|---|---|
| المؤلفون: | Pierre-Marie Choinier, Linda Broer, Jinghong Wan, Marcelle Bens, Emmanuel Weiss, Morgane Mabire, Sanae Ben Mkaddem, Sophie Lotersztajn, Patrice Codogno, Richard Moreau, Renato C. Monteiro, Tristan Thibault-Sogorb, Loredana Saveanu, Pushpa Hegde, Hélène Gilgenkrantz |
| المصدر: | Autophagy |
| بيانات النشر: | Informa UK Limited, 2020. |
| سنة النشر: | 2020 |
| مصطلحات موضوعية: | Liver Cirrhosis, 0301 basic medicine, Cirrhosis, Phagocytosis, Inflammation, Biology, Systemic inflammation, 03 medical and health sciences, Liver disease, medicine, Humans, Macrophage, Myeloid Cells, Molecular Biology, 030102 biochemistry & molecular biology, Monocyte, digestive, oral, and skin physiology, Autophagy, Cell Biology, medicine.disease, Autophagic Punctum, 3. Good health, 030104 developmental biology, medicine.anatomical_structure, Cancer research, medicine.symptom, Microtubule-Associated Proteins, human activities, Signal Transduction |
| الوصف: | Control of systemic and hepatic inflammation, in particular originating from monocytes/macrophages, is crucial to prevent liver fibrosis and its progression to end-stage cirrhosis. LC3-associated phagocytosis (LAP) is a non-canonical form of autophagy that shifts the monocyte/macrophage phenotype to an anti-inflammatory phenotype. In a recent study, we uncovered LAP as a protective mechanism against inflammation-driven liver fibrosis and systemic inflammation in the context of cirrhosis. We observed that LAP is enhanced in blood and liver monocytes from patients with liver fibrosis or those who progress to cirrhosis. Combining studies in which LAP was pharmacologically or genetically inactivated, we found that LAP limits inflammation in monocytes from cirrhotic patients, and the hepatic inflammatory profile in mice with chronic liver injury, resulting in anti-fibrogenic effects. Mechanistically, LAP-induced anti-inflammatory and antifibrogenic signaling results from enhanced expression of the Fc immunoreceptor FCGR2A/FcγRIIA and activation of an FCGR2A-mediated PTPN6/SHP-1 anti-inflammatory pathway, leading to increased engulfment of IgG into LC3 (+) phagosomes. In patients with cirrhosis progressing to multi-organ failure (acute-on chronic liver failure), LAP is lost in monocytes, and can be restored by targeting FCGR2A-mediated PTPN6/SHP-1 signaling. These data suggest that sustaining LAP may open novel therapeutic perspectives for patients with end-stage liver disease. |
| تدمد: | 1554-8635 1554-8627 |
| الوصول الحر: | https://explore.openaire.eu/search/publication?articleId=doi_dedup___::dfe2721d025c4c00a42db6689fc503f7Test https://doi.org/10.1080/15548627.2020.1770979Test |
| حقوق: | OPEN |
| رقم الانضمام: | edsair.doi.dedup.....dfe2721d025c4c00a42db6689fc503f7 |
| قاعدة البيانات: | OpenAIRE |
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LC3-associated phagocytosis (LAP) is a non-canonical form of autophagy that shifts the monocyte/macrophage phenotype to an anti-inflammatory phenotype. In a recent study, we uncovered LAP as a protective mechanism against inflammation-driven liver fibrosis and systemic inflammation in the context of cirrhosis. We observed that LAP is enhanced in blood and liver monocytes from patients with liver fibrosis or those who progress to cirrhosis. Combining studies in which LAP was pharmacologically or genetically inactivated, we found that LAP limits inflammation in monocytes from cirrhotic patients, and the hepatic inflammatory profile in mice with chronic liver injury, resulting in anti-fibrogenic effects. Mechanistically, LAP-induced anti-inflammatory and antifibrogenic signaling results from enhanced expression of the Fc immunoreceptor FCGR2A/FcγRIIA and activation of an FCGR2A-mediated PTPN6/SHP-1 anti-inflammatory pathway, leading to increased engulfment of IgG into LC3 (+) phagosomes. 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