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Psoriasis is a chronic skin disease mediated by Th17 and/or Th1 cells. Tim-3 is a cell surface molecule preferentially expressed on Th17 and Th1 cells. The interaction of Tim-3 with Tim-3 ligand inhibits cytokine production. To assess whether T cells in psoriasis have functional abnormalities, expression of cell surface Tim-3 on blood T cells producing interleukin-17 (Th17/Tc17 cells) or interferon-γ (Th1/Tc1 cells) was examined by flow cytometry. Psoriasis patients had higher numbers of Th17 and Tc17 cells, as well as Th1 and Tc1 cells, than healthy donors. However, Th17, Th1 and Tc1 cells in psoriasis did not efficiently express Tim-3 upon activation, compared with those from atopic dermatitis and healthy donors. Tim-3- cells showed more potent cytokine production than Tim-3+ cells. Impaired Tim-3 expression allows Th17, Th1 and Tc1 cells to escape from Tim-3-mediated negative regulatory systems and may contribute to the pathogenesis of psoriasis.

An 8-year-old boy presented with hydroa vacciniforme with recurrent oral mucosal ulcers and treatment-resistant gingivitis/periodontitis. Symptoms of oral mucosal involvement and gingivitis/periodontitis mirrored the severity of the skin lesions in sun-exposed areas. Although Epstein-Barr virus was negative in the skin lesions, Epstein-Barr virus DNA was detected in the gingival lesions when skin disease activity increased. Human herpes viruses-6 and -7 were also positive in the gingival lesions. Notably, human parvovirus B19 DNA was detected in both skin and gingival lesions. Impairment of systemic immunity was not detected. This report describes a rare case of hydroa vacciniforme with mucosal involvement and periodontal disease accompanied by multiple local virus re-activation.

Eosinophilic pustular folliculitis is an inflammatory skin disease characterized by pruritic follicular papulopustules. It is usually resistant to topical and/or systemic corticosteroids, but it responds well to systemic indomethacin. We report here two patients with classical-type disease who were treated with systemic indomethacin. As indomethacin is an inhibitor of cyclo-oxygenases and a potent agonist of the prostaglandin D2 (PGD2) receptor, CRTH2 (chemoattractant receptor homologous molecule expressed on Th2 cells), we investigated the effects of indomethacin on CRTH2 expression by leukocytes. CRTH2 was expressed on blood eosinophils and lymphocytes. In vitro treatment with indomethacin suppressed the expression of CRTH2 on these cells. In addition, systemic treatment with indomethacin reduced eosinophil CRTH2 expression in another patient in association with improvement of skin lesions and blood eosinophilia. A number of inflammatory cells expressed haematopoietic PGD synthase, an essential enzyme for generating PGD2 in skin lesions of eosinophilic pustular folliculitis. A PGD2-CRTH2 interaction may be involved in the pathogenesis. Moreover, indomethacin may exert its therapeutic effect via reducing CRTH2 expression, as well as by inhibiting PGD2 synthesis.

Dystrophic calcification in the skin occurs in association with a variety of disorders. To determine the association between subcutaneous calcification and chronic venous insufficiency, X-ray examinations were performed in 20 patients with chronic venous insufficiency and in 20 control subjects to detect latent calcification in their lower legs. Of the 20 patients, 13 (65%) had subcutaneous calcification, and the prevalence appeared to increase with disease duration, while only 4 control subjects (20%) had minimal calcification. Two types of calcification were identified based on their radiographic features: punctate and trabecular/reticular types. Patients with trabecular/reticular calcification had longer disease duration and more severe clinical scores than patients with punctate calcification. None of the control subjects had trabecular/reticular types of calcification. The identification of the presence and progression of latent calcification in the lower legs is useful, and may be necessary for the long-term management of chronic venous insufficiency, since calcification of skin tissues impedes wound healing and can be a risk factor for refractory ulcers.

Atopy patch testing with Japanese cedar pollen extract has been used to investigate patients with atopic dermatitis whose condition is exacerbated by contact with Japanese cedar pollen. Comparative atopy patch testing, scratch tests, and assays for total IgE and specific IgE were performed in 74 patients with atopic dermatitis, 5 patients with Japanese cedar pollinosis and 15 control subjects. A skin biopsy was performed on any sites that were positive to Japanese cedar pollen patch test. The results after 48 h of atopy patch testing were compared with the patient's history, skin scratch test and specific IgE. Twenty-two of the 74 patients (30%) had a history of exacerbation every spring after contact with Japanese cedar. Of these patients 68% showed a positive reaction to Japanese cedar pollen extract, as did 21% of patients with atopic dermatitis without a history of exacerbation by Japanese cedar pollen, 20% of patients with Japanese cedar pollinosis without eruption and 7% of control subjects. A histological examination revealed eczematous changes and infiltration of lymphocytes and eosinophils in atopy patch testing positive sites. In conclusion, atopy patch testing with Japanese cedar pollen extract is a useful method for investigating trigger factors for eczematous skin lesions in a subgroup of patients with atopic dermatitis.

Urticaria is characterized by transient wheals. We report here five cases with long-lasting urticarial lesions persisting for more than 24 hours. Each lesion left purpura after fading. There was no systemic involvement. C-reactive protein and serum levels of complement were elevated or normal. Histologically, marked infiltration by eosinophils and neutrophils with karyorrhexis in the perivascular and intercollagenous spaces was observed, but there was no evidence of vasculitis (venulitis). Skin symptoms were resistant to systemic corticosteroids. In contrast, treatment of underlying bacterial infections resulted in marked improvement of skin lesions. E-selectin, VCAM-1 and ICAM-1 were expressed on endothelial cells. Marked deposition of C3a, C5a, neutrophil elastase and major basic protein in the dermis was observed. These urticarial lesions provoked by bacterial infections seem to lie on the continuum between urticaria and urticarial vasculitis.

A case of eccrine porocarcinoma with Bowenoid changes is reported. We compared the results of immunohistochemical staining for epithelial membrane antigen in the present case with results in Bowen's disease to determine whether the presence of epithelial membrane antigen (EMA) enabled us to differentiate between Bowen's disease and eccrine porocarcinoma with Bowenoid changes. Histologically, the present tumour was characterized by atypical clear cells with Bowenoid changes as well as uniform small cells and intradermal nests with ductal structures. The membrane and cytoplasm of uniform small cells and ductal luminal surfaces were positive for EMA. However, the atypical cells with Bowenoid changes were negative for this. In contrast, tumour cells in Bowen's disease were positive for EMA. Although EMA is known to be a useful marker for some benign tumours derived from eccrine ducts, we found it difficult to distinguish eccrine porocarcinoma with Bowenoid changes from Bowen's disease using immunohistochemical staining for EMA.