Ontogeny of S-100 protein-positive histiocytes and lymphocytes in the human fetal lymphoreticular system.

In the human lymphoreticular system, the alpha and beta subunits of S-100 protein are found in ordinary monocyte-macrophages and non-phagocytic histiocytes such as Langerhans cells and interdigitating reticulum cells, respectively. The beta subunit is also present in some CD8+ T cells. In the present study, we investigated the ontogeny of these histiocytes and lymphocytes in humans. Yolk sacs and 4 to 21-week fetuses were examined immunohistochemically for the presence of S-100 protein subunits using antisera monospecific to each subunit. S-100 alpha + macrophages were present in the yolk sacs and the hepatic sinusoids of the 4th week embryos prior to bone marrow hematopoiesis. These macrophages later appeared in other lymphoid organs when anlagen of these organs were formed. No S-100 beta + cells were found in the yolk sacs. S-100 beta+ histiocytes were first detected in the hepatic sinusoids of the 5th week embryo, and after the 8th week of gestation, they were distributed in other lymphoid organs. S-100 beta+ lymphocytes were not found in the liver. They were first detected in the thymus at the 12th week of gestation, and were subsequently distributed in other lymphoid organs. These results suggest that S-100 beta+ lymphocytes and histiocytes may belong to different cell lineages, and the former may not be the precursor of the latter.</p

人胎児期，新生児期，幼児期，成人期造血における巨核球面積の変動

It has been reported that the appearance of small megakaryocytes can be detected in　various blood diseases and in fetal hematopoiesis. In the studies reported herein, we have investigated the age changes in the area of　megakaryocytes during fetal stage to the newborn infant, infant, and adult stage. The megakaryocyte increased in size from ago of 5 months to 10 months in fetal　stage, and then at the age of one year after birth reached a size almost identical to that　of adults. In comparing the megakaryocyte area by fetal age, however, the significant difference　was not observed in the hepatic and the bone marrow hematopoiesis at the age of 5　and 7 months. The results in comparing the area ratio of the nucleus to the cytoplasm of megakaryocytes　indicated that the nucleus of fetel megakaryocytes is generally smaller than that　of adult marrow megakaryocytes. This finding suggests that the size of the nucleus of megakaryocytes enlarges with　increase in the area of megakaryocytes. It is also considered that the functional or morphological changes of megakaryocytes　may reflect the function or morphology of the platelet

Neutrophil infiltration and oxidant-production in human atherosclerotic carotid plaques

To clarify the clinical implications of neutrophils in vulnerable plaques we evaluated the function and activity of infiltrated neutrophils in an atherosclerotic plaque, focusing on oxidant production. A histopathological investigation was performed using carotid arterial samples obtained from seven patients. The atherosclerotic plaques were examined cytochemically for naphthol-ASD-chloroacetate esterase activity and oxidant-production, and immunohistochemically using N-formyl peptide receptor-like 1 (fPRL1)-, CD66b-, CD68- or p22phox-specific antibodies. The cytoplasmic fPRL1 intensity value of the neutrophils in the plaque was estimated using an activity index. Naphthol-ASD-chloroacetate esterase activity was found in cells located in the atherosclerotic plaque, indicating that the cells were neutrophils. The cytoplasmic fPRL1 intensity value of the neutrophils in the plaque decreased to approximately 60% of the intensity observed in the capillary vessels. Oxidantproduction was also detected in the plaques, and both neutrophils and macrophages were observed at the corresponding oxidant-production sites. p22phox expression was also located in the same areas in which oxidant-production was observed in these plaques. We could not directly evaluate how much ROS generated from the infiltrated neutrophils contributed the plaque vulnerability followed by its rupture. However, the infiltrated neutrophils in the atherosclerotic plaques morphologically appeared activated and were actively generating oxidant, implying that neutrophils, together with macrophages, infiltrate into atherosclerotic plaques and contribute to plaque vulnerability