Lookup NU author(s): Dr Henrique De Paula Lemos,
Dr Lei Huang,
Professor Andrew Mellor
This work is licensed under a Creative Commons Attribution 4.0 International License (CC BY 4.0).
© 2017 Zhu et al. This is an open access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. Carbidopa is a drug that blocks conversion of levodopa to dopamine outside of central nervous system (CNS) and thus inhibits unwanted side effects of levodopa on organs located outside of CNS during management of Parkinson’s Disease (PD). PD is associated with increased expression of inflammatory genes in peripheral and central nervous system (CNS), infiltration of immune cells into brain, and increased numbers of activated/memory T cells. Animal models of PD have shown a critical role of T cells in inducing pathology in CNS. However, the effect of carbidopa on T cell responses in vivo is unknown. In this report, we show that carbidopa strongly inhibited T cell activation in vitro and in vivo. Accordingly, carbidopa mitigated myelin oligodendrocyte glycoprotein peptide fragment 35–55 (MOG-35-55) induced experimental autoimmune encephalitis (EAE) and collagen induced arthritis in animal models. The data presented here suggest that in addition to blocking peripheral conversion of levodopa, carbidopa may inhibit T cell responses in PD individuals and implicate a potential therapeutic use of carbidopa in suppression of T cell mediated pathologies.
Author(s): Zhu H, Lemos H, Bhatt B, Islam BN, Singh A, Gurav A, Huang L, Browning DD, Mellor A, Fulzele S, Singh N
Publication type: Article
Publication status: Published
Journal: PLoS ONE
Online publication date: 12/09/2017
Acceptance date: 28/06/2017
Date deposited: 23/10/2017
ISSN (electronic): 1932-6203
Publisher: Public Library of Science
Altmetrics provided by Altmetric