Mechanisms of spatial and temporal development of autoimmune vitiligo in tyrosinase-specific TCR transgenic mice.

摘要: Generalized vitiligo is thought to have an autoimmune etiology and has been correlated with the presence of CD8 T cells specific for melanocyte differentiation Ag. However, limited animal models disease hampered its understanding. Thus, we generated TCR transgenic mice that recognize epitope protein, tyrosinase. These animals develop strikingly similar characteristics human disease. Vitiligo develops temporally spatially, juvenile lesions forming bilaterally in head facial areas, only arising later body adult animals. entirely dependent on cells, whereas CD4 exert a negative regulatory effect. Importantly, can be pervasively present skin steady state without inducing most areas. This points developmental differences susceptibility and/or immunological effector mechanisms over time, or different locations. Disease strongly both IFN-γ CXCR3, dependence CCR5 more limited, CCR4 perforin are dispensable. Genetic ablation CXCR3 also resulted scarce cell infiltration into skin. Our results identify unexpected complexity development point toward possible therapeutic interventions.