This response was impaired in mice lacking IFNAR, the type I IFN receptor 11
The mechanism of aggression is based on the production of inflammatory cytokines such as TNF and IFN, in addition to the release of granzymes and perforins, which cause direct damage to melanocytes.78,80 In the lymphocytic infiltrate of the periphery of the depigmented areas, CD8+ T-lymphocytes predominate, and this finding correlates with disease activity.81 Melanocyte-specific antigens recognized by CD8+ T-cells, such as MelanA, tyrosinase, gp100, and tyrosinase-related proteins 1 and 2, are detected in greater numbers in the peripheral blood of patients with vitiligo when compared to controls.82 The perilesional skin also expresses higher levels of CD8+ T lymphocytes against melanocyte antigens in comparison to normal skin.78 These autoreactive cells are able to destroy melanocytes in vitro81 in addition to inducing apoptosis of keratinocytes and melanocytes in a pattern similar to the disease.78 IFN, and the genes it induces, encode the CXCR3 chemokine receptor and its ligands CXCL9 and CXCL10, which are critical for the activation of CD8+ T cells, and are found to be increased in the skin and blood of patients with vitiligo.83,84 CXCL9 promotes the global recruitment of autoreactive T-cells but with no effector action, whereas CXCL10 is required for disease progression and maintenance.85 Moreover, the neutralization of CXCL10 in animal models prevents the appearance of new lesions and induces the repigmentation of established areas,85 identifying the therapeutic potential of IFN/CXCL10/CXCR3 axis inhibition.86 Keratinocytes are the main sources of these cytokines, and CXCL9 and CXCL10 measurements are potential biomarkers of disease activity.84 The Janus kinase/signal transducers and transcription activators (JAK/STAT) pathway participate in the immunopathogenesis of vitiligo through its interaction with IFN
663 YuskaitisC
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