FRINK Linked Data Fragments server

Matches in SemOpenAlex for { <https://semopenalex.org/work/W2078633109> ?p ?o ?g. }

• W2078633109 abstract "Mesenchymal stem cells (MSCs) are adult, multipotent, stem cells with immunomodulatory properties. The mechanisms involved in the capacity of MSCs to inhibit the proliferation of proinflammatory T lymphocytes, which appear responsible for causing autoimmune disease, have yet to be fully elucidated. One of the underlying mechanisms studied recently is the ability of MSCs to generate T regulatory (Treg) cells in vitro and in vivo from activated peripheral blood mononuclear cells (PBMC), T-CD4+ and also T-CD8+ cells. In the present work we investigated the capacity of MSCs to generate Treg cells using T-CD4+ cells induced to differentiate toward the proinflammatory Th1 and Th17 lineages. MSCs were obtained from mouse bone marrow and characterized according to their surface antigen expression and their multilineage differentiation potential. CD4+ T cells isolated from mouse spleens were induced to differentiate into Th1 or Th17 cells and co-cultured with MSCs added at day 0, 2 or 4 of the differentiation processes. After six days, CD25, Foxp3, IL-17 and IFN-γ expression was assessed by flow cytometry and helios and neuropilin 1 mRNA levels were assessed by RT-qPCR. For the functional assays, the ‘conditioned’ subpopulation generated in the presence of MSCs was cultured with concanavalin A-activated CD4+ T cells labeled with carboxyfluorescein succinimidyl ester. Finally, we used the encephalomyelitis autoimmune diseases (EAE) mouse model, in which mice were injected with MSCs at day 18 and 30 after immunization. At day 50, the mice were euthanized and draining lymph nodes were extracted for Th1, Th17 and Treg detection by flow cytometry. MSCs were able to suppress the proliferation, activation and differentiation of CD4+ T cells induced to differentiate into Th1 and Th17 cells. This substantial suppressive effect was associated with an increase of the percentage of functional induced CD4+CD25+Foxp3+ regulatory T cells and IL-10 secretion. However, using mature Th1 or Th17 cells our results demonstrated that while MSCs suppress the proliferation and phenotype of mature Th1 and Th17 cells they did not generate Treg cells. Finally, we showed that the beneficial effect observed following MSC injection in an EAE mouse model was associated with the suppression of Th17 cells and an increase in the percentage of CD4+CD25+Foxp3+ T lymphocytes when administrated at early stages of the disease. This study demonstrated that MSCs contribute to the generation of an immunosuppressive environment via the inhibition of proinflammatory T cells and the induction of T cells with a regulatory phenotype. Together, these results might have important clinical implications for inflammatory and autoimmune diseases." @default.
• W2078633109 created "2016-06-24" @default.
• W2078633109 creator A5004895259 @default.
• W2078633109 creator A5015961928 @default.
• W2078633109 creator A5017549810 @default.
• W2078633109 creator A5024605869 @default.
• W2078633109 creator A5025907859 @default.
• W2078633109 creator A5044106964 @default.
• W2078633109 creator A5058103666 @default.
• W2078633109 creator A5065641562 @default.
• W2078633109 creator A5069087828 @default.
• W2078633109 creator A5071329217 @default.
• W2078633109 creator A5091010781 @default.
• W2078633109 date "2013-06-04" @default.
• W2078633109 modified "2023-10-17" @default.
• W2078633109 title "Mesenchymal stem cells generate a CD4+CD25+Foxp3+ regulatory T cell population during the differentiation process of Th1 and Th17 cells" @default.
• W2078633109 cites W1497240165 @default.
• W2078633109 cites W1640854798 @default.
• W2078633109 cites W1968159361 @default.
• W2078633109 cites W1972746775 @default.
• W2078633109 cites W1980910300 @default.
• W2078633109 cites W1985429617 @default.
• W2078633109 cites W2011653132 @default.
• W2078633109 cites W2024326908 @default.
• W2078633109 cites W2025294489 @default.
• W2078633109 cites W2030653181 @default.
• W2078633109 cites W2034875062 @default.
• W2078633109 cites W2038217510 @default.
• W2078633109 cites W2044875340 @default.
• W2078633109 cites W2047604189 @default.
• W2078633109 cites W2052271935 @default.
• W2078633109 cites W2054274983 @default.
• W2078633109 cites W2055273904 @default.
• W2078633109 cites W2063764243 @default.
• W2078633109 cites W2077005332 @default.
• W2078633109 cites W2089663997 @default.
• W2078633109 cites W2095666785 @default.
• W2078633109 cites W2097792324 @default.
• W2078633109 cites W2106072740 @default.
• W2078633109 cites W2106117542 @default.
• W2078633109 cites W2106471879 @default.
• W2078633109 cites W2112103893 @default.
• W2078633109 cites W2115788075 @default.
• W2078633109 cites W2122174032 @default.
• W2078633109 cites W2136586552 @default.
• W2078633109 cites W2144337206 @default.
• W2078633109 cites W2147638016 @default.
• W2078633109 cites W2159999899 @default.
• W2078633109 cites W2162819001 @default.
• W2078633109 cites W4295836001 @default.
• W2078633109 doi "https://doi.org/10.1186/scrt216" @default.
• W2078633109 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/3706898" @default.
• W2078633109 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/23734780" @default.
• W2078633109 hasPublicationYear "2013" @default.
• W2078633109 type Work @default.
• W2078633109 sameAs 2078633109 @default.
• W2078633109 citedByCount "350" @default.
• W2078633109 countsByYear W20786331092013 @default.
• W2078633109 countsByYear W20786331092014 @default.
• W2078633109 countsByYear W20786331092015 @default.
• W2078633109 countsByYear W20786331092016 @default.
• W2078633109 countsByYear W20786331092017 @default.
• W2078633109 countsByYear W20786331092018 @default.
• W2078633109 countsByYear W20786331092019 @default.
• W2078633109 countsByYear W20786331092020 @default.
• W2078633109 countsByYear W20786331092021 @default.
• W2078633109 countsByYear W20786331092022 @default.
• W2078633109 countsByYear W20786331092023 @default.
• W2078633109 crossrefType "journal-article" @default.
• W2078633109 hasAuthorship W2078633109A5004895259 @default.
• W2078633109 hasAuthorship W2078633109A5015961928 @default.
• W2078633109 hasAuthorship W2078633109A5017549810 @default.
• W2078633109 hasAuthorship W2078633109A5024605869 @default.
• W2078633109 hasAuthorship W2078633109A5025907859 @default.
• W2078633109 hasAuthorship W2078633109A5044106964 @default.
• W2078633109 hasAuthorship W2078633109A5058103666 @default.
• W2078633109 hasAuthorship W2078633109A5065641562 @default.
• W2078633109 hasAuthorship W2078633109A5069087828 @default.
• W2078633109 hasAuthorship W2078633109A5071329217 @default.
• W2078633109 hasAuthorship W2078633109A5091010781 @default.
• W2078633109 hasBestOaLocation W20786331091 @default.
• W2078633109 hasConcept C198826908 @default.
• W2078633109 hasConcept C203014093 @default.
• W2078633109 hasConcept C2776090121 @default.
• W2078633109 hasConcept C2778296632 @default.
• W2078633109 hasConcept C2778486448 @default.
• W2078633109 hasConcept C2779727006 @default.
• W2078633109 hasConcept C2780007613 @default.
• W2078633109 hasConcept C28328180 @default.
• W2078633109 hasConcept C2908647359 @default.
• W2078633109 hasConcept C71924100 @default.
• W2078633109 hasConcept C79484868 @default.
• W2078633109 hasConcept C86803240 @default.
• W2078633109 hasConcept C8891405 @default.
• W2078633109 hasConcept C95444343 @default.
• W2078633109 hasConcept C99454951 @default.
• W2078633109 hasConceptScore W2078633109C198826908 @default.
• W2078633109 hasConceptScore W2078633109C203014093 @default.
• W2078633109 hasConceptScore W2078633109C2776090121 @default.
• W2078633109 hasConceptScore W2078633109C2778296632 @default.

• next