Class II major histocompatibility antigen expression on coronary arterial endothelium in a patient with Kawasaki disease.

To investigate the class II major histocompatibility antigen expression on coronary arterial endothelium of Kawasaki disease and immunophenotypes of the infiltrating cells in the coronary vascular lesions, myocardial sections from a patient who died during the acute stage of Kawasaki disease were studied using an immunoperoxidase technique. The mononuclear cells in the lesions mainly consisted of macrophages and T cells, whereas B cells and NK/K cells were not seen. The majority of T cells reacted with Leu-3a antibodies, and only a few reacted with Leu-2a antibodies. Cells bearing the interleukin-2 receptor, indicative of activated T cells, were also found in the lesions. To determine the distribution of class II antigen, we used anti-HLA-DR antibodies. The massive expression of HLA-DR antigen on mononuclear cells was found in the lesions. In addition, the HLA-DR activation antigen was expressed on the coronary arterial endothelium at the infiltrates in which macrophages and T cells coexisted. In contrast, coronary arterial endothelium did not express HLA-DR antigens in the myocardial tissues of controls (n = 4). HLA-DR+ endothelial cells may play an important role in the development of Kawasaki vasculitis.

[Ureteral malacoplakia: a case report].

Malacoplakia is a condition which occurs most often in the urogenital system, but ureteral malacoplakia is rare. A case of ureteral malacoplakia is presented. The patients was a 54-year-old woman admitted to our hospital with high fever as the chief complaint. Laboratory data suggested urinary tract infection. Escherichia coli were isolated from the urine. Ultrasonography indicated left hydronephrosis and excretory urography showed reduced function of the left kidney. From retrograde pyelography, obstruction of the left distal ureter was indicated. A ureteral carcinoma was suspected and nephroureterectomy was thus carried out. The histopathological diagnosis was malacoplakia. The patient is in good health without any indication of the disease at 1 year 9 months following surgery.

M-spondin, a novel ECM protein highly homologous to vertebrate F-spondin, is localized at the muscle attachment sites in the Drosophila embryo.

The muscle attachment site (MAS) in Drosophila provides a unique and excellent model system to study the mechanism of cell-matrix adhesion in developing organisms. Here, we report on the isolation and characterization of a novel extracellular matrix (ECM) molecule localized at the MAS, encoded by the M-spondin (mspo) gene. M-spondin protein contains a thrombospondin type I repeat (TSR) previously found in a variety of ECM molecules. Furthermore, it shares two conserved domains with F-spondin, a vertebrate ECM molecule with TSRs. The presence of TSR(s) and the two homologous domains thus defines a novel gene family of ECM molecules. The mspo mRNA was expressed by a large subset of muscles in the embryonic body wall. Secreted M-spondin protein diffused and eventually became immobilized at the MAS in late embryos. When expressed in S2 cells, the protein was secreted and became concentrated in the matrix on the surface of the culture dish. Genetic analysis revealed that both deletion mutants and misexpression mutants suffered no obvious developmental defects. We propose that M-spondin, although its function is redundant, is a component of the ECM and mediates mechanical linkage between the muscles and apodemes.