title: Conditioned medium from adipose tissue-derived mesenchymal stem cells induces CD4+FOXP3+ cells and increases IL-10 secretion.
abstract: Mesenchymal stem cells (MSCs) are a new and promising tool for therapy of autoimmune disorders. In recent years their possibility to take part in the modulation of the immune response is discussed. The exact mechanisms for immunoregulation realized by MSCs are not clear yet, but interactions with other immunoregulatory cells may be involved in this process. The investigation of the influence of MSCs on the expression of FoxP3 and cytokine secretion by T helper cells was the aim of this study. T helper cells were isolated from PBMCs by magnetic separation and MSCs were isolated from human adipose tissue, and CD4⁺ T cells were cultured with conditional medium of MSCs. The methods which were used include flow cytometry, ELISA, and Human Proteome profiler kits. The results demonstrated that secretory factors in MSCs conditional medium lead to increased expression of FoxP3 and increased secretion of IL-10 by T helpers. The obtained results give us opportunity to discuss the interaction between two kinds of immunoregulatory cells: MSCs and FoxP3⁺ T helpers. We suppose that this interaction leads to increased number of immunosuppressive helpers which secrete IL-10. MSCs provide some of their immunosuppressive functions acting on T regulatory cells, and we believe that IL-6 secreted by MSCs is involved in this process.
authors.affiliation: Laboratory of Clinical Immunology, University Hospital "St. Ivan Rilski," Medical University of Sofia, 15 Acad. Ivan Geshov Street, 1431 Sofia, Bulgaria.
authors.forename: Ekaterina
authors.initials: E
authors.lastname: Ivanova-Todorova
authors.forename: Ivan
authors.initials: I
authors.lastname: Bochev
authors.forename: Rumen
authors.initials: R
authors.lastname: Dimitrov
authors.forename: Kalina
authors.initials: K
authors.lastname: Belemezova
authors.forename: Milena
authors.initials: M
authors.lastname: Mourdjeva
authors.forename: Stanimir
authors.initials: S
authors.lastname: Kyurkchiev
authors.forename: Plamen
authors.initials: P
authors.lastname: Kinov
authors.forename: Iskra
authors.initials: I
authors.lastname: Altankova
authors.forename: Dobroslav
authors.initials: D
authors.lastname: Kyurkchiev
mesh_terms: D000273:Adipose Tissue / Q000166:cytology*; D017209:Apoptosis / Q000187:drug effects / Q000276:immunology; D015496:CD4-Positive T-Lymphocytes / Q000166:cytology* / Q000187:drug effects / Q000276:immunology / Q000378:metabolism*; D002478:Cells, Cultured; D018925:Chemokines / Q000378:metabolism; D017077:Culture Media, Conditioned / Q000494:pharmacology*; D051858:Forkhead Transcription Factors / Q000378:metabolism*; D006801:Humans; D016753:Interleukin-10 / Q000378:metabolism*; D053645:Interleukin-2 Receptor alpha Subunit / Q000378:metabolism; D015850:Interleukin-6 / Q000378:metabolism; D018655:Lymphocyte Count; D059630:Mesenchymal Stem Cells / Q000166:cytology* / Q000187:drug effects; D006377:T-Lymphocytes, Helper-Inducer / Q000166:cytology / Q000187:drug effects / Q000378:metabolism; D015854:Up-Regulation / Q000187:drug effects
chemical_list: D018925:Chemokines; D017077:Culture Media, Conditioned; C418974:FOXP3 protein, human; D051858:Forkhead Transcription Factors; C508609:IL10 protein, human; C508600:IL6 protein, human; D053645:Interleukin-2 Receptor alpha Subunit; D015850:Interleukin-6; D016753:Interleukin-10