sirolimus has been researched along with Vitiligo* in 3 studies
3 other study(ies) available for sirolimus and Vitiligo
| Article | Year |
|---|---|
Polymeric nanoparticles containing rapamycin and autoantigen induce antigen-specific immunological tolerance for preventing vitiligo in mice.
Vitiligo is an autoimmune disease in which pigment is lost in patches of the skin. CD4 Topics: Animals; Autoantigens; Dendritic Cells; Mice; Nanoparticles; Sirolimus; Vitiligo | 2021 |
Novel approaches to vitiligo treatment via modulation of mTOR and NF-κB pathways in human skin melanocytes.
Topics: alpha-MSH; Blotting, Western; Cells, Cultured; Chromones; Humans; Hydrogen Peroxide; Melanocytes; Microscopy, Confocal; Morpholines; NF-kappa B; Phosphatidylinositol 3-Kinases; Phosphoinositide-3 Kinase Inhibitors; Sirolimus; TOR Serine-Threonine Kinases; Tumor Necrosis Factor-alpha; Vitiligo | 2017 |
A quantitative increase in regulatory T cells controls development of vitiligo.
T-cell cytolytic activity targeting epidermal melanocytes is shown to cause progressive depigmentation and autoimmune vitiligo. By using the recently developed transgenic mice h3TA2 that carry T cells with a HLA-A2-restricted human tyrosinase peptide (h-Tyr)-reactive TCR and develop spontaneous vitiligo from an early age, we addressed the mechanism regulating autoimmune vitiligo. Depigmentation was significantly impaired only in IFN-γ-knockout h3TA2 mice but not in TNF-α- or perforin-knockout h3TA2 mouse strains, confirming a central role for IFN-γ in vitiligo development. In addition, regulatory T cells (Tregs) were relatively abundant in h3TA2-IFN-γ(-/-) mice, and depletion of the Treg-engaging anti-CD25 antibody fully restored the depigmentation phenotype in h3TA2-IFN-γ(-/-) mice, mediated in part through the upregulation of proinflammatory cytokines such as IL-17 and IL-22. Further therapeutic potential of Treg abundance in preventing progressive depigmentation was evaluated by adoptively transferring purified Treg or using rapamycin. Both the adoptive transfer of Tregs and the use of rapamycin induced a lasting remission of vitiligo in mice treated at the onset of disease, or in mice with established disease. This leads us to conclude that reduced regulatory responses are pivotal to the development of vitiligo in disease-prone mice, and that a quantitative increase in the Treg population may be therapeutic for vitiligo patients with active disease. Topics: Adoptive Transfer; Animals; Autoimmunity; Disease Progression; Epidermal Cells; Epidermis; Female; Humans; Immunosuppressive Agents; Interferon-gamma; Male; Melanocytes; Mice; Mice, Inbred C57BL; Mice, Knockout; Mice, Transgenic; Receptors, CCR5; Receptors, CXCR3; Sirolimus; T-Lymphocyte Subsets; T-Lymphocytes, Regulatory; Tumor Necrosis Factor-alpha; Vitiligo | 2014 |