| Literature DB >> 34561224 |
Marie Eliane Azoury1, Fatoumata Samassa1, Mijke Buitinga2, Laura Nigi3, Noemi Brusco3, Aïsha Callebaut2, Matthieu Giraud4, Magali Irla5, Ana Ines Lalanne1, Alexia Carré1, Georgia Afonso1, Zhicheng Zhou1, Barbara Brandao1, Maikel L Colli6, Guido Sebastiani3, Francesco Dotta3, Maki Nakayama7, Decio L Eizirik6,8, Sylvaine You1, Sheena Pinto9, Mark J Mamula10, Yann Verdier11, Joelle Vinh11, Soren Buus12, Chantal Mathieu2, Lut Overbergh2, Roberto Mallone13,14.
Abstract
In type 1 diabetes, autoimmune β-cell destruction may be favored by neoantigens harboring posttranslational modifications (PTMs) such as citrullination. We studied the recognition of native and citrullinated glucose-regulated protein (GRP)78 peptides by CD8+ T cells. Citrullination modulated T-cell recognition and, to a lesser extent, HLA-A2 binding. GRP78-reactive CD8+ T cells circulated at similar frequencies in healthy donors and donors with type 1 diabetes and preferentially recognized either native or citrullinated versions, without cross-reactivity. Rather, the preference for native GRP78 epitopes was associated with CD8+ T cells cross-reactive with bacterial mimotopes. In the pancreas, a dominant GRP78 peptide was instead preferentially recognized when citrullinated. To further clarify these recognition patterns, we considered the possibility of citrullination in the thymus. Citrullinating peptidylarginine deiminase (Padi) enzymes were expressed in murine and human medullary epithelial cells (mTECs), with citrullinated proteins detected in murine mTECs. However, Padi2 and Padi4 expression was diminished in mature mTECs from NOD mice versus C57BL/6 mice. We conclude that, on one hand, the CD8+ T cell preference for native GRP78 peptides may be shaped by cross-reactivity with bacterial mimotopes. On the other hand, PTMs may not invariably favor loss of tolerance because thymic citrullination, although impaired in NOD mice, may drive deletion of citrulline-reactive T cells.Entities:
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Year: 2021 PMID: 34561224 PMCID: PMC8660990 DOI: 10.2337/db21-0259
Source DB: PubMed Journal: Diabetes ISSN: 0012-1797 Impact factor: 9.461