Vascular Changes in Bleomycin-Induced Scleroderma

Systemic sclerosis (SSc) is characterized by vascular injury, immunological abnormalities, and fibrosis of the skin as well as various internal organs. Vascular impairment is the early manifestation and plays a fundamental role in the pathogenesis of SSc. Recent studies suggest that complex interactions among the endothelial cells, pericytes, smooth muscle cells, and fibroblasts are involved in the systemic vasculopathy in SSc, and histological feature of proliferation of vascular wall is seen in the lesional scleroderma skin at the late stage of disease. One of the most representative mouse models for scleroderma is the bleomycin-induced scleroderma; however, aspects of vascular alteration have not been described in detail so far. A number of studies have shown that bleomycin stimulates endothelial cells and fibroblasts to induce proinflammatory and fibrogenic cytokines, apoptosis, reactive oxygen species, and so on. This paper makes a focus on the vascular involvement in the bleomycin-induced murine scleroderma

Nonsegmental Vitiligo and Autoimmune Mechanism

Nonsegmental vitiligo is a depigmented skin disorder showing acquired, progressive, and depigmented lesions of the skin, mucosa, and hair. It is believed to be caused mainly by the autoimmune loss of melanocytes from the involved areas. It is frequently associated with other autoimmune diseases, particularly autoimmune thyroid diseases including Hashimoto's thyroiditis and Graves' disease, rheumatoid arthritis, type 1 diabetes, psoriasis, pernicious anemia, systemic lupus erythematosus, Addison's disease, and alopecia areata. This indicates the presence of genetically determined susceptibility to not only vitiligo but also to other autoimmune disorders. Here, we summarize current understanding of autoimmune pathogenesis in non-segmental vitiligo

Serum Anti-BPAG1 Auto-Antibody Is a Novel Marker for Human Melanoma

Malignant melanoma is one of the most aggressive types of tumor. Because malignant melanoma is difficult to treat once it has metastasized, early detection and treatment are essential. The search for reliable biomarkers of early-stage melanoma, therefore, has received much attention. By using a novel method of screening tumor antigens and their auto-antibodies, we identified bullous pemphigoid antigen 1 (BPAG1) as a melanoma antigen recognized by its auto-antibody. BPAG1 is an auto-antigen in the skin disease bullous pemphigoid (BP) and anti-BPAG1 auto-antibodies are detectable in sera from BP patients and are used for BP diagnosis. However, BPAG1 has been viewed as predominantly a keratinocyte-associated protein and a relationship between BPAG1 expression and melanoma has not been previously reported. In the present study, we show that bpag1 is expressed in the mouse F10 melanoma cell line in vitro and F10 melanoma tumors in vivo and that BPAG1 is expressed in human melanoma cell lines (A375 and G361) and normal human melanocytes. Moreover, the levels of anti-BPAG1 auto-antibodies in the sera of melanoma patients were significantly higher than in the sera of healthy volunteers (p<0.01). Furthermore, anti-BPAG1 auto-antibodies were detected in melanoma patients at both early and advanced stages of disease. Here, we report anti-BPAG1 auto-antibodies as a promising marker for the diagnosis of melanoma, and we discuss the significance of the detection of such auto-antibodies in cancer biology and patients

Significance of MDR1-Gene and P-Glycoprotein (P-gp) Expressions in the Lesional Skin of Psoriasis Vulgaris

We have examined P-gp (P-glycoprotein) and multi-drug resistance 1 (MDR1) gene expressions in the lesional skin of psoriasis vulgaris and atopic dermatitis some of those showed a decreased clinical response to topical corticosteroid ointment during the clinical course. The patients were subdivided into four groups; S (-): responder to topical steroid without steroid ointment for one month at the time of biopsy, S (+): responder to topical steroid and under steroid therapy at the time of biopsy, R (-): low or non- responder to topical steroid without steroid therapy for one month at the time of biopsy, R (+): low-or non-responder to topical steroid and under steroid therapy at the time of biopsy. P-gp was mainly expressed in the cytoplasm of some epidermal keratinocytes and most of infiltrating cells in the dermis of the lesional skin of psoriasis or atopic dermatitis. Scores of P-gp protein-expression was significantly higher in the patients under steroid ointment both in psoriasis vulgaris and atopic dermatitis. While R (+) group showed much more intense expression of P-gp than S (+) group in psoriasis vulgaris but this was not the case for atopic dermatitis. MDR1 gene was expressed in the lesional skin of R (+) psoriasis but not in S (+) psoriasis or normal skin. These results suggest that steroid-resistance occasionally experienced in psoriasis vulgaris might be related to the overexpression of P-gp which is possibly induced after topical steroid ointment. This might provide a new insight for the mechanism of steroid -insensitivity in inflammatory skin disorders especially in psoriasis vulgaris

An Extremely Rare Case of Leukoderma Induced by Cosmetics Containing Ascorbic Acid

We report the case of a 73-year-old woman with leukoderma induced by cosmetics containing ascorbic acid. She had noticed the sudden appearance of a hypopigmented macule on the cheek within 1 month after use of the cosmetics with the brand name Obaji C Serum. No history of use of rhododenol-containing cosmetics was declared. Histopathological analysis revealed that the number of matured melanocytes was apparently decreased, and T lymphocytes abundantly infiltrated mainly the perifollicular region. In addition to the discontinuation of using Obaji C Serum, phototherapy by excimer light was noticeably effective for repigmentation. To our knowledge, there has been no other report so far showing hypopigmented lesions induced by this cosmetic