[Anetoderma Schwenninger-Buzzi in a dark-skinned patient]. / Anetodermie Schwenninger-Buzzi auf dunkler Haut.

A 10-year-old boy in Uganda developed primary anetoderma (Schwenninger-Buzzi). It is important not to confuse anetoderma with BL leprosy in spite of some superficial resemblance of the two diseases. Primary anetoderma is probably extremely rare in patients with dark skin although this may partly be due to a lack of dermatologists in Africa who could diagnose the disease.

[Cutaneous manifestation of cysticercosis]. / Kutane Manifestation der Zystizerkose.

Cysticercosis, an infection with the larva of Taenia solium, is caused by the accidental ingestion of the parasite's eggs. In many countries of the Third World, cysticercosis, and especially neurocysticercosis, is a widespread problem. A patient from Northern Malawi presented not only with cysticercosis but also with BT leprosy and pityriasis versicolor. Dermatologists should be familiar with the clinical picture of cysticercosis in order to make an early diagnosis in patients from at-risk areas.

MHC-derived peptides and the CD4+ T-cell repertoire: implications for autoimmune disease.

The receptor repertoire of peripheral CD4+ cells is primarily determined by selection processes in the thymus. These result in the positive selection of T cells whose receptors weakly recognize self-peptides restricted by class II self-MHC heterodimers. A majority of such self-peptide partial agonists are likely to be derived from self-MHC molecules. It is suggested that these thymically selected, weakly autoreactive T cells may subsequently be stimulated by peripheral exposure to microbially derived agonists that 'mimic' corresponding self-MHC peptides. In turn, 'molecular mimicry' between microbial agonists and tissue-specific self-peptides may lead to T-cell-mediated autoimmune disease. Hence such disease may reflect 'three-way mimicry' between peptides of respectively target tissue, pathogen and self-MHC (or other self-peptide dominantly presented in the thymus). This hypothesis accounts for the role of MHC haplotype in determining susceptibility to (or protection from) autoimmune disease. Direct evidence is presented in favour of the model as applied to diseases such as rheumatoid arthritis, autoimmune uveitus and autoimmune diabetes. Strong circumstantial evidence, based primarily on sequence similarities, is also presented for other autoimmune diseases. However, it is noted that the statistics of database searches, and the lack of predictable correlation between sequence similarity and T-cell cross-reactivity, require that such evidence be substantiated by further direct experiment.