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Frozen sections of 52 breast carcinomas were examined for the presence and nature of a leukocytic infiltrate. The number of "common leukocyte (T200-) antigen"-bearing cells was remarkably high in the stromal compartment of the carcinomas, whereas the tumor foci themselves were usually infiltrated only sparsely. Approximately 80% of these T200+ stromal cells carried the myelomonocyte lineage-associated antigens M-M522 and 63D3 and exhibited "non-specific esterase" activity. More than 2/3 of the stromal monocytic cells expressed the T4 antigen as verified by monoclonal antibodies (MAbs) directed against different T4-associated epitopes. A T-cell analysis showed that T4+ cells clearly outweighed the total number of T cells as defined by anti-T3 and anti-TII antibodies. In addition, a correlation became apparent between the HLA-DR phenotype and the T lymphocyte content of tumor cell areas in the sense that densely infiltrated tumor areas were invariably HLA-DR+.

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A 5-month-old boy died of progressive heart failure that started at the age of 3 months. Autopsy revealed a mitochondrial cardiomyopathy and a mitochondrial myopathy of the limb muscle and diaphragm. Cytochemically random defects of cytochrome c oxidase were visualized by light and electron microscopy in the diaphragm and especially the heart muscle, the limb muscle showing a diffuse attenuation whereas the liver and kidneys reacted normally. The activities of NADH-dehydrogenase (complex I) and cytochrome c oxidase (complex IV) were severely diminished (20% residual activity of controls) in the skeletal and heart muscle. In the heart, succinate cytochrome c reductase (complex II/III) was additionally decreased to the same degree. Loss of cytochrome c oxidase activity was based on a reduction of both mitochondrial and nuclear derived subunits in the heart and diaphragm as revealed by immunohistochemical analysis, whereas the limb muscle showed a normal immunoreactive protein content. The results illustrate heterogeneous tissue expression of respiratory chain enzyme defects and demonstrate that a cardiomyopathy may be the leading presentation of a mitochondrial disorder in early infancy.