Anti-inflammaging effects of human alpha-1 antitrypsin

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Anti‐inflammaging effects of human alpha‐1 antitrypsin

Inflammaging plays an important role in most age-related diseases. However, the mechanism of inflammaging is largely unknown, and therapeutic control of inflammaging is challenging. Human alpha-1 antitrypsin (hAAT) has immune-regulatory, anti-inflammatory, and cytoprotective properties as demonstrated in several disease models including type 1 diabetes, arthritis, lupus, osteoporosis, and strok...

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Immune-modulating effects of alpha-1 antitrypsin.

Alpha-1 antitrypsin (AAT) is a circulating serine protease inhibitor (serpin) that inhibits neutrophil elastase in the lung, and AAT deficiency is associated with early-onset emphysema. AAT is also a liver-derived acute-phase protein that, in vitro and in vivo, reduces production of pro-inflammatory cytokines, inhibits apoptosis, blocks leukocyte degranulation and migration, and modulates local...

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Alpha 1-antitrypsin in human macrophages.

Preliminary studies have suggested that alpha-1-antitrypsin (A1AT) is a useful immunohistochemical marker of histiocytes (monocytes/macrophages) and malignant tumours derived from them. To confirm the reliability of this marker a wide variety of benign and malignant lymphoreticular cells and tissues have been stained by the immunoperoxidase technique for A1AT and positive staining was found to ...

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Alpha 1 antitrypsin deficiency.

Alpha-1 antitrypsin deficiency is an inherited disorder that may cause severe lung and liver disease.

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Alpha 1-Antitrypsin Does Not Inhibit Human Monocyte Caspase-1

BACKGROUND Alpha 1-antitrypsin (A1AT) is a 52 kDa serine protease inhibitor produced largely by hepatocytes but also by mononuclear phagocytes. A1AT chiefly inhibits neutrophil elastase and proteinase-3 but has also been reported to have immune modulatory functions including the ability to inhibit caspases. Its clinical availability for infusion suggests that A1AT therapy might modulate caspase...

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ژورنال

عنوان ژورنال: Aging Cell

سال: 2017

ISSN: 1474-9718

DOI: 10.1111/acel.12694