Upregulation of Tolerogenic Pathways by the Hydrogen Sulfide Donor GYY4137 and Impaired Expression of H2S-Producing Enzymes in Multiple Sclerosis.
2020
Аутори:
Lazarević, MilicaBattaglia, Giuseppe
Jevtić, Bojan
Nikolovski, Neda
Bruno, Valeria
Cavalli, Eugenio
Miljković, Đorđe
Nicoletti, Ferdinando
Momčilović, Miljana
Fagone, Paolo
Тип документа:
Чланак у часопису (Објављена верзија)
Метаподаци
Приказ свих података о документуАпстракт:
The aim of this study was to examine the in vitro effects of the slow-releasing H2S donor GYY4137 on the immune cells involved in the pathogenesis of the central nervous system (CNS) autoimmune disease, multiple sclerosis (MS). GYY4137 specifically potentiated TGF-β expression and production in dendritic cells and significantly reduced IFN-γ and IL-17 production in the lymph node and spinal cord T cells obtained from mice immunized with CNS antigens. Both the proportion of FoxP3+ regulatory CD4+ T cells in the lymph node cells, and the percentage of IL-17+ CD4+ T cells in the spinal cord cells were reduced upon culturing with GYY4137. Interestingly, the peripheral blood mononuclear cells obtained from the MS patients had a lower expression of the H2S-producing enzyme, 3-mercaptopyruvate-sulfurtransferase (MPST), in comparison to those obtained from healthy donors. A significant inverse correlation between the expression of MPST and several pro-inflammatory factors was also observed. Further studies on the relevance of the observed results for the pathogenesis and therapy of MS are warranted.
Кључне речи:
T cells; Carbon monoxide; Dendritic cells; Experimental autoimmune encephalomyelitis; Hydrogen sulfide; Multiple sclerosis; Nitric oxide; Regulatory T cellsИзвор:
Antioxidants (Basel, Switzerland), 2020, 9, 7, 608-Финансирање / пројекти:
- Министарство науке, технолошког развоја и иновација Републике Србије, институционално финансирање - 200007 (Универзитет у Београду, Институт за биолошка истраживања 'Синиша Станковић') (RS-MESTD-inst-2020-200007)
DOI: 10.3390/antiox9070608
ISSN: 2076-3921
PubMed: 32664399
WoS: 000558340200001
Scopus: 2-s2.0-85087811841
URI
https://www.mdpi.com/2076-3921/9/7/608http://www.ncbi.nlm.nih.gov/pubmed/32664399
https://radar.ibiss.bg.ac.rs/handle/123456789/3819