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Lookup NU author(s): Emeritus Professor Andrew MellorORCiD
This work is licensed under a Creative Commons Attribution 4.0 International License (CC BY 4.0).
The epididymis maintains a state of immune tolerance towards spermatozoa while also protecting them and itself against infection and acute inflammation. The immunosuppressive enzyme indoleamine 2,3-dioxygenase 1 (Ido1) participates in this delicate local equilibrium. Using the mouse Ido1−/− model, we show here that the absence of IDO1 expression leads in the epididymis but not in serum to (1) an increase in the inflammatory state as evidenced by changes in the content of cytokines and chemokines, (2) the engagement of a Th1-driven inflammatory response as evidenced by changes in the Th17/Treg as well as Th1/Th2 equilibria, as well as (3) differences in the content of lipid intermediates classically involved in inflammation. Despite this more pronounced inflammatory state, Ido1−/− animals succeed in preserving the local epididymal immune situation due to the activation of compensatory mechanisms that are discussed.
Author(s): Jrad-Lamine A, Henry-Berger J, Damon-Soubeyrand C, Saez F, Kocer A, Janny L, Pons-Rejraji H, Munn DH, Mellor AL, Gharbi N, Cadet R, Aitken RJ, Drevet JR
Publication type: Article
Publication status: Published
Journal: PLoS ONE
Year: 2013
Volume: 8
Issue: 6
Online publication date: 20/06/2013
Date deposited: 20/03/2019
ISSN (electronic): 1932-6203
Publisher: Public Library of Science
URL: https://doi.org/10.1371/journal.pone.0066494
DOI: 10.1371/journal.pone.0066494
PubMed id: 23840489
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