Martín-Saavedra, Francisco MGonzález-García, CoralBravo, BeatrizBallester, Sara2023-02-142023-02-142008-09Mol Immunol. 2008 Sep;45(15):4008-19.0161-5890http://hdl.handle.net/20.500.12105/15504Beta-interferon (IFN-beta) is a valuable therapy for multiple sclerosis (MS) which is also effective in the animal model of experimental autoimmune encephalomyelitis (EAE). However, the accurate mechanisms to explain its anti-inflammatory activity in the disease are not fully revealed. Available data support that T lymphocytes are among the main cell targets of IFN-beta. We have found that in vitro anti-CD3 stimulation of uncommitted murine naïve T cells under IFN-beta treatment results in skewing the T cell differentiation process towards the T2 phenotype, in a prevention from apoptosis of naturally occurring CD4+ T regulatory cells (nTreg) in correlation with an increase in Bcl-XL expression, and in a decrease of IL-17 expression. Elimination of nTreg from the primary culture of naïve CD4+ cells abolished the down-regulation of IL-17 driven by IFN-beta, what suggests the interaction between Th17 and nTreg subsets. Experiments in EAE induced in SJL mice, showed in vivo evidence for the accumulation of spleen CD4+CD25+GITR+Foxp3+ cells after IFN-beta treatment. On the other hand, treated animals showed a striking decrease of IL-17 expression by peripheral CD4+ cells (Th17) and MBP-specific spinal cord cells. Both the in vivo and in vitro results point out new targets through which IFN-beta could exert its therapeutic action.engAMEAEIL-4IL-17Foxp3nTregIFN-BetaAnimalsCD4-Positive T-LymphocytesCell DifferentiationCells, CulturedInterferon-betaInterleukin-17MiceMice, Inbred C3HSpleenT-Lymphocytes, RegulatoryTh2 CellsAttribution-NonCommercial-NoDerivatives 4.0 Internacional1863993445154008-1910.1016/j.molimm.2008.06.006Molecular immunologyopen access