Advances in genome-wide association studies (GWASs) have highlighted the heterogeneous nature of autoimmune diseases (1), conditions whereby malfunctioning of molecular mechanisms underlying tolerance translates into the activation of autoreactive immune cells. Immune checkpoint molecules are regulators of the immune system that preserve self-tolerance and prevent autoimmunity. Indoleamine 2,3-dioxygenase 1 (IDO1) is a metabolic enzyme that acts as immune checkpoint molecule and is characterized by common single-nucleotide polymorphisms (SNPs), all detectable in noncoding regions of the IDO1 gene (2). Among these, the CC genotype at IDO1 rs7820268 is associated with impaired IDO1 activity in peripheral blood mononuclear cells (PBMCs) from children with autoimmune diabetes and with an enhanced risk of developing the disease (3). Full … [↵][1]1To whom correspondence may be addressed. Email: ursula.grohmann{at}unipg.it or claudia.volpi{at}unipg.it. [1]: #xref-corresp-1-1
Reply to Han et al.: On track for an IDO1-based personalized therapy in autoimmunity
G. Mondanelli,A. Carvalho,P. Puccetti,U. Grohmann,C. Volpi
Published 2020 in Proceedings of the National Academy of Sciences of the United States of America
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- Publication year
2020
- Venue
Proceedings of the National Academy of Sciences of the United States of America
- Publication date
2020-09-29
- Fields of study
Medicine
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Semantic Scholar, PubMed
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