Low HLA binding of diabetes-associated CD8+ T-cell epitopes is increased by post translational modifications.

ABSTRACT:

Background

Type 1 diabetes (T1D) is thought to be an autoimmune disease driven by anti-islet antigen responses and mediated by T-cells. Recent published data suggests that T-cell reactivity to modified peptides, effectively neoantigens, may promote T1D. These findings have given more credence to the concept that T1D may not be solely an error of immune recognition but may be propagated by errors in protein processing or in modifications to endogenous peptides occurring as result of hyperglycemia, endoplasmic reticulum (ER) stress, or general beta cell dysfunction. In the current study, we hypothesized that diabetes-associated epitopes bound human leukocyte antigen (HLA) class I poorly and that post-translational modifications (PTM) to key sequences within the insulin-B chain enhanc

SUBMITTER: Sidney J 

PROVIDER: S-EPMC5863483 | biostudies-literature | 2018 Mar

REPOSITORIES: biostudies-literature