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The role of endoplasmic reticulum stress in autoimmune-mediated beta-cell destruction in type 1 diabetes.
Pinkse, G.G. et al. Autoreactive CD8 T cells associated with beta cell destruction in type 1 diabetes.
Identification of epitopes that are recognized by diabetogenic T cells and cause selective beta cell destruction in type 1 diabetes (T1D) has focused on peptides originating from native beta cell proteins.
Autoimmune mechanisms are of main importance for β-cell destruction in type 1 diabetes.
This indicates that inhibition of Bim and Puma, or their inducers, may prevent beta-cell destruction in type 2 diabetes.
Endoplasmic reticulum stress mediated decline of β-cells in WSD occurs earlier in life than autoimmune-mediated β-cell destruction in type 1 diabetes.
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Pathological studies have revealed common features, including islet inflammation and β-cell destruction, in both type 1 and type 2 diabetes [ 34, 40].
Joosten, L. A. B. et al. Il-1αβ blockade prevents cartilage and bone destruction in murine type II collagen-induced arthritis, whereas TNF-α blockade only ameliorates joint inflammation.
Pathological scoring of immune invasion and joint destruction in wild type (WT) and peptidyl arginine deiminase 4 knockout (PAD4 KO) K/BxN mice.
Securin destruction in wild-type [ 12] or Cdc20f/f oocytes is blocked by nocodazole.
Oxidative stress plays a permissive role in the process of apoptosis leading to cell destruction in many types of cell lineages [ 6, 7].
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