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CXCL10 is critical for the progression and maintenance of depigmentation in a mouse model of vitiligo.
Innate immune mechanisms in vitiligo: danger from within.
Simvastatin prevents and reverses depigmentation in a mouse model of vitiligo.
Keratinocyte-Derived Chemokines Orchestrate T-Cell Positioning in the Epidermis during Vitiligo and May Serve as Biomarkers of Disease.
A double-blind, placebo-controlled, phase-II clinical trial to evaluate oral simvastatin as a treatment for vitiligo.
CXCR3 Depleting Antibodies Prevent and Reverse Vitiligo in Mice.
Suction blistering the lesional skin of vitiligo patients reveals useful biomarkers of disease activity.
Antibody blockade of IL-15 signaling has the potential to durably reverse vitiligo.
Resident Memory and Recirculating Memory T Cells Cooperate to Maintain Disease in a Mouse Model of Vitiligo.
Mouse Model for Human Vitiligo.
Jak Inhibitors Reverse Vitiligo in Mice but Do Not Deplete Skin Resident Memory T Cells.
Type I interferon signaling limits viral vector priming of CD8+ T cells during initiation of vitiligo and melanoma immunotherapy.
Case Series: Gene Expression Analysis in Canine Vogt-Koyanagi-Harada/Uveodermatologic Syndrome and Vitiligo Reveals Conserved Immunopathogenesis Pathways Between Dog and Human Autoimmune Pigmentary Disorders.
A Keratinocyte-Tethered Biologic Enables Location-Precise Treatment in Mouse Vitiligo.
Lesional CD8+ T-Cell Number Predicts Surgical Outcomes of Melanocyte-Keratinocyte Transplantation Surgery for Vitiligo.
Rational design of a JAK1-selective siRNA inhibitor for the modulation of autoimmunity in the skin.