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Gedde- Dahl T Jr (1971) Epidermolysis Bullosa: A Clinical, Genetic and Epidemiological Study. The Johns Hopkins University Press: Baltimore, MD Janda L, Damborsky J, Rezniczek GA et al. (2001) Plectin repeats and modules: strategic cysteines and their presumed impact on cytolinker functions. Bioessays 23:1064-9 Kiritsi D, Pigors M, Tantcheva-Poor I et al. (2013) Epidermolysis bullosa simplex Ogna revisited. J Invest Dermatol 133:270-3 Koss-Harnes D, Hoyheim B, Anton-Lamprecht I et al. (2002) A site-specific plectin mutation causes dominant epidermolysis bullosa simplex Ogna: two identical de novo mutations. J Invest Dermatol 118:87-93 Koss-Harnes D, Jahnsen FL, Wiche G et al. (1997) Plectin abnormality in epidermolysis bullosa simplex Ogna: non-responsiveness of basal keratinocytes to some anti-rat plectin antibodies. Exp Dermatol 6:41-8 Koster J, van Wilpe S, Kuikman I et al. (2004) Role of binding of plectin to the integrin beta4 subunit in the assembly of hemidesmosomes.

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Purpose: Superficial dermatophytosis is quite commonly seen in patients with adult T-cell leukemia/ lymphoma (ATLL), as approximately 50% of the patients develop cutaneous mycotic infections. Because superficially infected fungi in the stratum corneum of the epidermis cannot directly contact with T cells infiltrating in the upper dermis, some perturbation of epidermal innate immunity has been postulated. Interleukin (IL)-17-producing helper T cells (Th17) can induce the keratinocyte production of antimicrobial peptides such as human b defensin (HBD)-2 and LL-37, which play an essential role in cutaneous innate immunity.Experimental Design: We investigated the frequency of circulating Th17 cells, serum levels of cytokines, and epidermal expression of HBD-1, 2, 3, and LL-37 in ATLL patients with or without superficial dermatophytosis.Results: The frequency of peripheral Th17 cells and the serum level of IL-17 was significantly decreased in ATLL patients, whereas the serum IL-10 and TGF-b1 levels were increased as compared with healthy controls. Furthermore, ATLL patients with dermatophytosis had higher IL-10 and TGF-b1 levels and lower IL-17 levels than did those without dermatophytosis. Immunohistochemical study revealed that the epidermal expression of both HBD-2 and LL-37 were significantly lower in ATLL patients with dermatophytosis than in non-ATLL patients with dermatophytosis.Conclusions: Taken together, these results suggest that the keratinocyte production of antimicrobial peptides promoted by Th17 cells is reduced in ATLL patients, leading to the perturbed innate immunity and the frequent occurrence of superficial dermatophytosis.

Urocanic acid (UCA) is an epidermal chromophore that undergoes trans to cis isomerization after UVB irradiation. cis-UCA is a potent inhibitor of cutaneous acquired immunity. The aim of this study was to explore the genes, which are upregulated by cis-UCA in normal human epidermal keratinocytes (NHEK) and investigated its role in vitro using human T-lymphocyte cell line, Jurkat cells. DNA microarray analysis and real-time PCR investigation revealed that cis-UCA, not trans-UCA, increased the expression of a gene encoding a b-galactoside-binding lectin, galectin-7, LGALS7B. Immunohistochemical study demonstrated that galectin-7 was highly expressed in the epidermis in the patients with actinic keratosis. Galectin-7 administration upregulated apoptosis and inhibited the expression of interleukin-2 (IL2) and interferon-c (IFNG) mRNA in Jurkat cells. Taken together, galectin-7 may play important roles in downregulating the functions of T lymphocytes after UVB irradiation and can be developed into novel immunosuppressive therapies for inflammatory skin diseases.