Please use this identifier to cite or link to this item:

TitleAmino acid metabolism as drug target in autoimmune diseases
Author(s)Mondanelli, Giada
Iacono, Alberta
Carvalho, Agostinho
Orabona, Ciriana
Volpi, Claudia
Pallotta, Maria T.
Matino, Davide
Esposito, Susanna
Grohmann, Ursula
KeywordsAmino Acids
Arginase 1
Autoimmune Diseases
Immunosuppressive Agents
Indoleamine 2,3-dioxygenase 1
Metabolic Networks and Pathways
Molecular Targeted Therapy
Arginine metabolism
Host genetics
Immune regulation
Tryptophan metabolism
Issue dateApr-2019
JournalAutoimmunity Reviews
Abstract(s)In mammals, amino acid metabolism has evolved to control immune responses. Autoimmune diseases are heterogeneous conditions that involve the breakdown of tolerogenic circuitries and consequent activation of autoreactive immune cells. Therefore, critical enzymes along amino acid degradative pathways may be hijacked to keep in check autoimmunity. We examined here current knowledge of indoleamine 2,3-dioxygenase 1 (IDO1) and arginase 1 (ARG1), the main enzymes catabolizing tryptophan and arginine, respectively, in organ-specific and systemic autoimmune diseases as well as in the development of autoantibodies to therapeutic proteins. At variance with neoplastic contexts, in which it is known to act as a pure immunosuppressive molecule, ARG1 exhibited a protective or pathogenetic profile, depending on the disease. In contrast, in several autoimmune conditions, the bulk of data indicated that drugs capable of potentiating IDO1 expression and activity may represent valuable therapeutic tools and that IDO1-based immunotherapeutic protocols could be more effective if tailored to the genetic profile of individual patients.
AccessOpen access
Appears in Collections:ICVS - Artigos em revistas internacionais / Papers in international journals

Files in This Item:
File Description SizeFormat 
Mondanelli G et al. Autoimmun Rev.pdf1,07 MBAdobe PDFView/Open

Partilhe no FacebookPartilhe no TwitterPartilhe no DeliciousPartilhe no LinkedInPartilhe no DiggAdicionar ao Google BookmarksPartilhe no MySpacePartilhe no Orkut
Exporte no formato BibTex mendeley Exporte no formato Endnote Adicione ao seu ORCID