Kaoru Takayama

Basophil recruitment and activation in inflammatory skin diseases

To cite this article: Ito Y, Satoh T, Takayama K, Miyagishi C, Walls AF, Yokozeki H. Basophil recruitment and activation in inflammatory skin diseases. Allergy 2011; 66: 1107–1113.

Japanese cedar pollen as an exacerbation factor in atopic dermatitis : Results of atopy patch testing and histological examination

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 patients 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.

Interferon-gamma differentially regulates CD80 (B7-1) and CD86 (B7-2/B70) expression on human Langerhans cells

CD80 (B7‐1) and CD86 (B7‐2/B70) have recently been identified in cultured human Langerhans cells (LCs), although their role and regulatory properties remain unclear. We present our comparison of the expression of the molecules, mRNAs and the function between CD80 and CD86 in human LCs treated by interferon γ (IFN‐γ). We examined the regulatory properties of CD80 and CD86 expression in human LCs pretreated with IFN‐γ. Flow cytometric analysis indicated that the mean fluorescence intensity of CD86 but not CD80 was enhanced. However, the percentage modulation of both CD80 and CD86 positive cells were significantly up‐regulated in a dose‐dependent manner, after 48‐h culturing with IFN‐γ. The regulatory properties of CD80 and CD86 mRNA expressions in human LC were studied using polymerase chain reaction methods. We found that both CD80 and CD86 mRNA of enriched LCs following IFN‐γ pretreatment for 12 h were higher than those without pretreatment.

Comparative analysis of CD80 and CD86 on human Langerhans cells: expression and function.

Abstract Although both CD80 (B7–1) and CD86 (B7–2/B70) have been recently identified in cultured human Langerhans cells (LC), little is known of the role and regulatory properties of CD80 and CD86 on human LC. We present here the results of a study comparing the expression and function of CD80 and CD86 in human LC using the T-helper type-1 cytokines IL-2 and interferonγ (IFN)-γ, and the T-helper type-2 cytokines IL-10, IL-4 and granulocyte/macrophage colony-stimulating factor (GM-CSF). Freshly isolated human LC expressed little CD80 and CD86 in vitro, but the expression of both molecules was rapidly induced during a 72-h incubation with cytokines and the expression of CD86 occurred much earlier and more strongly than that of CD80. The expression of both CD80 and CD86 was upregulated by GM-CSF and downregulated by IL-10, and the expression of CD86, but not that of CD80, was upregulated by both IL-4 and IFN-γ. Finally, pretreatment of LC with GM-CSF and IFN-γ, but not with IL-4, enhanced the alloreactive T-cell proliferation induced by the LC, and IL-10 pretreatment of LC decreased their capacity for alloreaction. These results indicate that the expression of both CD80 and CD86 on human LC may be regulated by these cytokines (IL-2, IL-4, GM-CSF, IFN-γ and IL-10) secreted from helper T cells infiltrating into the inflammatory microenvironment.

Taste Disorders in Healthy “Carriers” and “Non-Carriers” of Candida albicans and in Patients with Candidosis of the Tongue

Impairments in taste perception may be caused by a number of factors, including the presence of Candida albicans in the oral cavity. We attempted to establish whether the presence of Candida albicans on the tongue is a cause of taste disorders by studying taste disorders in patients with candidosis of the tongue and in healthy “carriers” and “non‐carriers” of C. albicans. Taste disorders and their severity were objectively assessed by the filter‐paper disk method in 18 patients with candidosis of the tongue and in 33 healthy “carriers” and 167 healthy “non‐carriers” of C. albicans. The gustatory function was re‐tested in 7 patients and 8 “carriers” after treatment with topical anti‐mycotic medication to detect any improvement. Patients with candidosis of the tongue and “carriers” of C. albicans demonstrated significantly higher incidences (p<0.001) of taste disorders than did “non‐carriers”. The mean taste threshold of each of the four individual taste qualities was significantly higher in patients with candidosis than in “non‐carriers”. The average taste threshold was significantly higher in “carriers” than in “non‐carriers”. Post‐treatment improvement or recovery from taste disorders was obtained in 5 out of 7 patients (71.4%) with candidosis and in 7 out of 8 “carriers” (87.5%) of C. albicans. This study clearly demonstrates that not only overt candidosis of the tongue but also commensal harboring of ***C. albicans is a cause of taste disorders.

A de novo missense mutation in the keratin 13 gene in oral white sponge naevus

White sponge naevus (WSN; OMIM 193900) is a rare autosomal dominant disorder characterized by variable, and at times extensive, leucokeratosis of the oral mucosa. In some cases, the nasal, oesophageal and anogenital mucosa may be similarly affected. Histologically, involved mucosa shows a characteristic basket-weave or cell-within-cell appearance. Recent study has shown that keratin 4 (K4) and keratin 13 (K13) gene mutations are associated with WSN. Thus far, four pathogenic mutations have been identified in K4 and five in K13 in patients with WSN, and all these mutations were identified in familial cases of WSN. Clinically, oral manifestations seen in WSN resemble those found in mucosal disorders such as lichen planus and candidiasis. Therefore, it is not always easy to diagnose a patient with sporadic WSN with no family history of the disorder. Here we report a novel de novo missense mutation in KRT13 identified in a sporadic case of WSN.

Dialysis-related Amyloidosis on the Buttocks

-microglobulin amyloidosis presenting as a pediculated dermal nodule and large subcutaneous masses on the buttocks.CASE REPORTA 69-year-old man presented with a few years’ history of nodules on the buttocks. Past history included chro-nic renal failure controlled with haemodialysis for 19 years and a decompression operation for carpal tunnel syndrome. Physical examination revealed a red-brown pediculated nodule 50×20 mm in diameter on the sacral region (Fig. 1A). In addition, 120×80 mm elastic, hard subcutaneous masses were palpable beneath the skin of the buttock. Laboratory findings showed increased levels of blood urea nitrogen (38 mg/dl; normal range 7–19 mg/dl), serum creatinine (6.5 mg/dl; normal range 0.5–0.8 mg/dl) and β

Methotrexate-related lymphoproliferative disorder with extensive vascular involvement in a patient with rheumatoid arthritis

We describe the development of a cutaneous lymphoproliferative disorder in a patient with rheumatoid arthritis who was treated with methotrexate. Skin manifestations were characterized by thrombophlebitis-like lesions and ulcerated nodules. Histologic examination revealed large polymorphic atypical cells including Reed-Sternberg-like cells expressing CD20 and CD30 in the dermis and subcutaneous tissues. Tumor cells infiltrated the walls of dermal arterioles, subcutaneous arteries, and veins, leading to the destruction of vascular structures. Activation of Epstein-Barr virus was detected. Skin lesions improved remarkably after the discontinuation of methotrexate. This case illustrates the rare occurrence of cutaneous vascular involvement in methotrexate-related lymphoproliferative disorder that did not require any specific chemotherapy.

Cowden syndrome: a novel mutation and overlooked glycogenic acanthosis in gingiva

Cowden syndrome (CS; OMIM 158350) is a rare genetic disorder that is characterized by multiple hamartomas (affecting various organs derived from all three germ layers) and an increased risk of some cancers, in particular thyroid and breast cancers. The lifetime risks for thyroid and breast cancer are estimated to be 3–10% and 25–50%, respectively. Characteristic mucocutaneous manifestations include multiple facial trichilemmomas, oral mucosal papillomatoses and acral keratoses. These clinical findings, as well as other hamartomatous or carcinomatous lesions, usually become evident in adulthood. CS is caused by mutations in the PTEN gene (phosphatase and tensin homologue deleted from chromosome 10), which encodes a dual phosphatase that signals down the phosphoinositol3-kinase ⁄Akt pathway and exerts G1 cell cycle arrest and apoptosis. PTEN mutations also cause a subset of Bannayan– Riley–Ruvalcaba syndrome (BRRS; OMIM 153480). BRRS has not been associated with malignant lesions. It was proposed that CS and BRRS result from germline mutations in a common gene (PTEN), and thus should be classified as PTEN hamartoma tumour syndromes (PHTS). The genetic mechanism by which mutations in a single gene cause such a diverse number of phenotypes is largely unknown. Here, we report a novel single nucleotide duplication in the PTEN gene in a de novo case of CS, in which mutational analysis was helpful in confirming the clinical diagnosis. Interestingly, in this case, the histopathological findings of mucosal papillomatosis contrasted with those that are generally recognized in cases of CS.

Psoriatic Skin Lesions Induced by BCG Vaccination

A 6-month-old girl presented with skin eruptions that appeared following BCG vaccination that had been carried out at a local public health centre. Plaques initially appeared on the vaccination site one month after vaccination, followed by the appearance of multiple plaques on the face and extremities during the next month. Physical examination revealed multiple red papules and well-defined plaques covered by whitishyellow scale/crust on the face and extremities, as well as at the site of BCG vaccination (Fig. lA-C). The nails of the fingers and toes showed subungual hyperkeratosis (Fig. ID). The patients medical history included congenital mitral valve insufficiency, and