The central lymphoid tissue in developmental immunobiology.
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Biomedical subjects
Publications and source records attributed to R A Good.
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When chimeric A strain mice tolerant of (A x C57BL/1)F(1) hybrid skin grafts are injected with spleen cells from normal A donors the recipients develop weight loss, clinical evidence of runting, and death in some animals. Similar recipients injected with spleen cells from A strain donors immunized against C57BL/1 tissue show a more rapid onset of the runting process and increased mortality. Runting in. these experiments therefore results from an immune attack by the injected A strain lymphoid cells against the (A x C57BL/1)F(1) hybrid tissue harbored by the chimeric recipients. Since the hybrid tissues of the chimeric recipients were derived from spleen cell populations we conclude that the immunologic rejection of lymphoid and hematopoietic tissue is sufficient to cause the runting syndrome. C3H mice tolerant of A strain skin grafts because of the prior injection of viable or disrupted A strain spleen material were given 400 r of x-irradiation and an injection of C3H spleen cells. Only the chimeric C3H mice harboring viable A strain cells developed weight loss and clinical evidence of disease, showing again that runting occurs only when an attack can be made against viable lymphoid and hematopoietic tissue. Normal A strain mice injected intravenously with 850 million (A x C57BL/1)F(1) hybrid spleen cells reject hybrid skin grafts and do not develop runting, whereas the rejection of similar hybrid tissue present in chimeric A strain mice results in runting. It is concluded that runting will occur only when the immunologic attack is directed against lymphoid and hematopoietic tissue which has become established within host tissues. The possibility that runting may result from hypersensitivity reactions occurring in the lymphoid tissues is discussed.
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A procedure was developed for the isolation from human bone marrow of a cell fraction enriched for haematopoietic precursors and depleted of T lymphocytes. T cells are eliminated from bone marrow by rosetting with sheep red blood cells, followed by differential agglutination of residual T lymphocytes in the non-rosetting population by the lectin, soybean agglutinin. The fraction unagglutinated by the lectin contains a high proportion of colony-forming cells and non detectable T cell alloreactivity in vitro. Similar results were obtained with monkey bone-marrow cells, suggesting that monkeys can be used for evaluation of this fractionation technique for bone-marrow transplantation across histocompatibility barriers.
Four adults, recently diagnosed, acute leukemic patients received 40 separate platelet transfusion treatments before, during, and after intravenous administration of amphotericin B. Fourteen of these platelet transfusions were administered while the patients also received amphotericin B; 26 platelet transfusions were given before or after amphotericin B therapy. The mean platelet increment for platelet transfusions administered while the patients were untreated with amphotericin B was 58 +/- 6 per cent. While the same patients were being treated with amphotericin B, the mean platelet increment was significantly decreased to 29 +/- 8 per cent (t = 3.1; p less than 0.005). In addition, when the patients were not being given amphotericin B, a highly significant negative relationship (r = -0.77; p less than 0.001) between the values for bleeding time and venous platelet count was present. In contrast, during amphotericin B treatment there was no correlation between the patients' bleeding times and venous platelet counts. We propose that amphotericin B therapy has a direct toxic effect on the function and circulation of transfused platelets. These toxic effects are quickly corrected by discontinuing this antifungal antibiotic.
Nineteen recently diagnosed patients with acute leukemias received prophylactic platelet transfusions when thrombocytopenic. Platelet concentrates were always transfused within eight hours of collection. The result of each transfusion was carefully monitored for the posttransfusion platelet increment. One patient died four days after admission to the present study. Seven patients died 1 to 14 months after the institution of antileukemic chemotherapy. Four patients received marrow transplants 1 to 2 months after starting chemotherapy and, therefore, were longer evaluated in this study. One patient was lost to follow-up after seven months of observation. The remaining six patients are alive and have been followed for 9 to 18 months. During the period of observation, none of the patients developed any evidence of refractoriness to platelet transfusion therapy. Although this series does not permit any firm conclusions to be made, it appears that the magnitude of the problem of alloimmunization to platelet transfusion therapy may be overemphasized.
Leser-Trélat Sign refers to a sudden showering of seborrheic keratoses and its possible relationship to internal malignancy.
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