Search Results - "Eliseeva, Daria D"
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Modulation of Suppressive Activity and Proliferation of Human Regulatory T Cells by Splice-Switching Oligonucleotides Targeting FoxP3 Pre-mRNA
Published in Cells (Basel, Switzerland) (29-12-2023)“…The maturation, development, and function of regulatory T cells (Tregs) are under the control of the crucial transcription factor Forkhead Box Protein 3…”
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Induction of FoxP3 Pre-mRNA Alternative Splicing to Enhance the Suppressive Activity of Regulatory T Cells from Amyotrophic Lateral Sclerosis Patients
Published in Biomedicines (01-05-2024)“…Forkhead box protein 3 (FoxP3) is a key transcription factor responsible for the development, maturation, and function of regulatory T cells (Tregs). The FoxP3…”
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Phenotypical and Functional Characteristics of Human Regulatory T Cells during Ex Vivo Maturation from CD4+ T Lymphocytes
Published in Applied sciences (01-07-2021)“…Regulatory T cells (Tregs) participate in the negative regulation of inflammatory reactions by suppressing effector cells. In a number of autoimmune disorders,…”
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Myelin Oligodendrocyte Glycoprotein as an Autoantigen in Inflammatory Demyelinating Diseases of the Central Nervous System
Published in Biochemistry (Moscow) (01-04-2023)“…Demyelinating diseases of the central nervous system are caused by an autoimmune attack on the myelin sheath surrounding axons. Myelin structural proteins…”
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Ex vivo expanded regulatory T cells CD4 + CD25 + FoxP3 + CD127 Low develop strong immunosuppressive activity in patients with remitting-relapsing multiple sclerosis
Published in Autoimmunity (Chur, Switzerland) (01-09-2016)“…Multiple sclerosis (MS) is an autoimmune disease characterized by defect in regulatory function of CD4 CD25 T cells. We demonstrated difference in proportion…”
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Ex vivo expanded regulatory T cells CD4+CD25+FoxP3+CD127Low develop strong immunosuppressive activity in patients with remitting-relapsing multiple sclerosis
Published in Autoimmunity (Chur, Switzerland) (01-09-2016)“…Multiple sclerosis (MS) is an autoimmune disease characterized by defect in regulatory function of CD4 + CD25 + T cells. We demonstrated difference in…”
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