Vitiligo Models

Autoimmune Nephropathy Models and Efficacy Services
IgA NephropathyC3 GlomerulonephritisLupus NephritisMembranous Nphropathy
Asthma Models and Efficacy Services
HDM induced asthma modelsOVA inudced asthma models
Systemic Lupus Erythematosus (SLE) Models and Efficacy Services
Spontaneous SLE ModelsInduction SLE ModelsImmune Reconstitution SLE Models
Sjögren's Syndrome Models and Efficacy Services
Salivary Gland Protein Induced Sjögren's Syndrome Mouse ModelSTING Agonist Induced Sjögren’s Syndrome Mouse Model
Neuroimmune Diseases Models and Efficacy Services
Multiple Sclerosis (MS) ModelsMyasthenia Gravis (MG) Models
Autoimmune Dermatoses Models and Efficacy Services
Psoriasis ModelsAtopic DermatitisAlopecia Areata (AA)Vitiligo ModelsSclerodermaUrticaria
Inflammatory Bowel Disease (IBD) Models and Efficacy Services
DSS Induced IBD ModelAdaptive T cell Transfer IBD ModelImmune Reconstitution IBD ModelAnti-CD40 Induced Colitis Models
Rheumatoid Arthritis (RA) Models and Efficacy Services
Collagen Induced Arthritis ModelCollagen Antibody Induced Arthritis ModelImmune Reconstitution Arthritis ModelmBSA induced Induced DTHA Model
Immune Reconstitution Autoimmune Disease Models and Efficacy Services
SLEIBDArthritisMyasthenia GravisPassive Cutaneous AnaphylaxisPassive Systemic Anaphylaxis (PSA)

Vitiligo is an autoimmune skin disease characterized by depigmented skin as a result of melanocyte loss. Additional clinical features of vitiligo include patchy loss of skin color, premature whitening of the hair, and loss of color in the tissues (mouth and nose). The exact cause of vitiligo remains unknown, but some possible factors include genetic causes and environmental triggers that results in autoreactive CD8+ T cells that target melanocytes . The disease is maintained by melanocyte-reactive resident memory T cells (Trm) cells through an IL-15 dependent signaling pathway.

 

1. Monobenzone-induced vitiligo model

Model strategy and features of Monobenzone-induced vitiligo model


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Phenotypic manifestations of Monobenzone-induced vitiligo model

 

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Ruxolitinib treatment was effective in treating depigmentation in animals induced by Monobenzone treatment .

 

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Skin HE

Representative H&E stains of each treatment group. G1: Control group; G2: Monobenzone induction group; G3: Monobenzone + 1.5% Ruxolitinib treatment group. Fibrous tissue hyperplasia (blue arrows), neutrophils (purple arrows), epidermal thickening (white arrows), punctate necrosis of the dermis (black arrows), lymphocytes (red arrows), hyperkeratosis (yellow arrows).


2. B16 melanoma tumor-induced autoreactive vitiligo model

Model strategy and features of B16 melanoma tumor-induced autoreactive vitiligo model

 

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Depigmentation score and incidence rate increased in treated mice. G2: Control group; G3: B16 melanoma-induced autoreactive vitiligo

 

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The percentage and number of CD8+ T cell in spleen, back skin and blood increased in G3 induced autoreactive vitiligo group. Data presented as mean±s.d. and analyzed using t-test. Statistical significance is denoted as follows: *p < 0.05, **p < 0.01, and ***p < 0.001.

 

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Mouse CD8/CXCL9/CXCL10/IFN-γ transcript levels were increased in G3 induced autoreactive vitiligo group. Data presented as mean±s.d. and analyzed using t-test. Statistical significance is denoted as follows: *p < 0.05, **p < 0.01, and ***p < 0.001.

 


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