| First Author | Riding RL | Year | 2021 |
| Journal | Pigment Cell Melanoma Res | Volume | 34 |
| Issue | 4 | Pages | 683-695 |
| PubMed ID | 33040466 | Mgi Jnum | J:353804 |
| Mgi Id | MGI:7716748 | Doi | 10.1111/pcmr.12935 |
| Citation | Riding RL, et al. (2021) Type I interferon signaling limits viral vector priming of CD8(+) T cells during initiation of vitiligo and melanoma immunotherapy. Pigment Cell Melanoma Res 34(4):683-695 |
| abstractText | Vitiligo is an autoimmune skin disease in which epidermal melanocytes are targeted for destruction by CD8(+) T cells specific for melanocyte/melanoma-shared antigens. IFNgamma is the central cytokine driving disease, but the role of type I IFN in vitiligo remains unclear. We investigated the functional role of type I IFN during vitiligo progression using two different mouse models: one induced with a vaccinia virus (VV) vaccine and one induced with dendritic cells to prime autoimmune T cells. Induction of vitiligo by VV in IFNaR-deficient mice led to the development of severe vitiligo compared with wild-type (WT) mice and was characterized by a significantly enhanced effector CD8(+) T-cell response. Severe vitiligo in this model was a result of VV persistence, because exacerbation of disease in IFNaR-deficient mice was not observed when antigen-pulsed dendritic cells were used to induce vitiligo instead of virus. Treatment of B16F10 melanoma-inoculated mice with VV vaccine therapy also induced a significantly enhanced anti-tumor response in IFNaR-deficient mice compared with WT. These results not only help define the pathways responsible for vitiligo progression but also suggest that blockade of type I IFNs following administration of a VV vaccine may provide increased immunogenicity and efficacy for melanoma immunotherapy. |
