Boris M. Baranovski

TL;DR: Non‐obvious developments in the understanding of AAT biology disqualify it from being a straightforward anti‐inflammatory agent: AAT does not block dendritic cell activities, nor does it promote viral and tumour susceptibilities, stunt B lymphocyte responses or render treated patients susceptible to infections; accordingly, outcomes of elevated AAT do not overlap those attained by immunosuppression.

TL;DR: HAAT significantly reduced infection-induced leukopenia and liver, pancreas, and lung injury, and it significantly improved 24-hour survival rates, suggesting that prolonged hAAT treatment in patients without hA AT deficiency is safe.

TL;DR: It is suggested that temporal T-cell depletion, as in the clinically practiced anti-thymocyte-globulin therapy, combined with hAAT, may promote islet xenograft acceptance.

TL;DR: In this article, the extracellular form of the abundant heat shock protein, gp96, is involved in human autoimmune pathologies, and α1-antitrypsin (AAT) is shown to be a regulator of gp96-mediated inflammatory responses, an increasingly appreciated endogenous damage response with relevance to human pathologies.

TL;DR: Evidence is provided that non‐nutrient factors in serum have a major impact on β‐cell mitochondrial adaptations to changes in metabolism, as indicated by CR‐mediated prevention of mitochondrial fusion arrest and reduced respiratory function in INS1 cells under glucolipotoxicity.