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Immune responses in a mouse model of vitiligo with spontaneous epidermal de‐ and repigmentation
Author(s) -
Eby Jonathan M.,
Kang HeeKap,
Klarquist Jared,
Chatterjee Shilpak,
Mosenson Jeffrey A.,
Nishimura Michael I.,
GarrettMayer Elizabeth,
Longley B. Jack,
Engelhard Victor H.,
Mehrotra Shikhar,
Le Poole I. Caroline
Publication year - 2014
Publication title -
pigment cell and melanoma research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.618
H-Index - 105
eISSN - 1755-148X
pISSN - 1755-1471
DOI - 10.1111/pcmr.12284
Subject(s) - vitiligo , transgene , genetically modified mouse , depigmentation , melanocyte , biology , immune system , immunology , filaggrin , t cell receptor , receptor , t cell , microbiology and biotechnology , cancer research , gene , genetics , atopic dermatitis , melanoma
Summary To generate a mouse model of spontaneous epidermal depigmentation, parental h3 TA 2 mice, expressing both a human‐derived, tyrosinase‐reactive T‐cell receptor on T cells and the matching HLA ‐A2 transgene, were crossed to keratin 14‐promoter driven, stem cell factor transgenic (K14‐ SCF ) mice with intra‐epidermal melanocytes. In resulting Vitesse mice, spontaneous skin depigmentation precedes symmetrical and sharply demarcated patches of graying hair. Whereas the SCF transgene alone dictates a greater retinoic acid receptor‐related orphan receptor gamma ( ROR γt) + T‐cell compartment, these cells displayed markedly increased IL ‐17 expression within Vitesse mice. Similar to patient skin, regulatory T cells were less abundant compared with K 14‐ SCF mice, with the exception of gradually appearing patches of repigmenting skin. The subtle repigmentation observed likely reflects resilient melanocytes that coexist with skin‐infiltrating, melanocyte‐reactive T cells. Similar repigmenting lesions were found in a different TCR transgenic model of vitiligo developed on an SCF transgenic background, supporting a role for SCF in repigmentation.