No abstract

SUMMARYThe distribution of TNF-a, p55 TNF reeeptor (TNF-R) and p75 TNF-R in normal skin and uninvolved and lesional skin from psoriasis patients has been investigated, using specific mono-and polyclonal antibodies. In normal skin, and uninvolved and lesional skin from psoriasis patients, p55 TNF-R is associated with epidermal keratinocytes and a network of upper dermal dendritic cells. This suggests that the actions oCTNF-a on epidermal ceNs/Hrn-o are mediated by binding to the p55 TNF-R. In Icsionat psoriasis skin, there was staining of the parakeratotic stratum eorneuni and increased expression of p55 TNF-R in association with upper dermal blood vessels. Staining for p75 TNF-R in normal skin was restricted to eccrine sweat ducts and dermal dendritic cells, and was absent from the epidermis. In lesional psoriasis skin, there was slaining for p75 TNF-R in association with upper dermal blood vessels and perivascular infiltrating cells. TNF-a in normal skin was predominantly localized to the basal cell layers ofthe epidermis, and was seen in association with eccrine ducts and sebaceous glands. In lesional psoriasis skin, and to a lesser extent in uninvolved psoriasis skin. TNF-a; was distributed throughout the epidermis, and was also specifically localized to upper dermal blood vessels. Up-regulation of TNF-a. p55 TNF-R and p75 TNF-R on dermal blood vessels in psoriasis may play an important role in the pathogenesis of this condition by promoting cutaneous recruitment of inflatiimatory cells.

No abstract

No abstract

No abstract

Five dark-skinned individuals presented with widespread well-demarcated hypopigmented lesions, biopsy of which revealed the histopathological features of mycosis fungoides. Ultrastructural studies showed focal invasion of the epidermis by mycosis cells with degenerative changes in adjacent melanocytes and keratinocytes. The majority of melanocytes exhibited swelling of cytoplasmic organelles and disordered melanogenesis with production of spherical incompletely melanized melanosomes. In addition disintegrating melanocytes were occasionally seen. Perifollicular repigmentation within hypopigmented areas occurred in two patients following clearing of the epidermal infiltrate with PUVA therapy. Mycosis fungoides may present with areas of cutaneous hypopigmentation.

No abstract

Human leukocyte antigen (HLA) associations have been reported in Amerindian patients with actinic prurigo. To determine if similar associations are present in the British Caucasoid population with actinic prurigo, 26 patients underwent serological typing for HLC Class I and II antigens. DNA analysis by both sequence-specific priming and group-specific amplification with single-stranded oligonucleotide probe hybridization was used to confirm the DR and DQ typing and to perform DR4 subtyping. All patients were DR4 positive, and 25 of 26 patients were DQ7 positive. DR4 subtyping revealed 12 of 20 patients tested to be DRB1*0407. A nonsignificant association was also found with HLA B55 that is in linkage disequilibrium with DRB1*0407. No HLA associations were found in 25 British Caucasoid patients with polymorphic light eruption. DRB1*0407 is rare in European Caucasoids without actinic prurigo, and HLA-DR4 may have an important role in determining expression of this disease.