A low density fraction of bone marrow cells enriched in prothymocyte activity.
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Biomedical subjects
S Ezine
Publications and source records attributed to S Ezine.
Repopulation potential of thymocytes forming rosettes with phagocytic cells of the thymic reticulum.
Thymocytes binding in vitro to phagocytic cells of the thymic reticulum (P-TR), termed 'rosetting thymocytes', were injected intravenously into irradiated congenic mice and their migration patterns were compared with those that do not bind to P-TR, called 'non-rosetting thymocytes', similarly transferred. Donor cells, C57BL/Ka Thy 1.2, were distinguished from recipient cells, C57BL/Ka Thy 1.1 by a direct immunofluorescence technique using an anti-Thy 1.2 monoclonal antibody. The results demonstrate that the rosetting thymocytes have a greater capacity for homing back to the thymus and for populating the mesenteric lymph node and the spleen. Intrathymic transfer assay revealed that the donor-derived cells detected in the peripheral organs were of thymic origin.
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The phenotype of thymocytes derived from a single clonogenic precursor.
Clonogenic repopulation of the thymus of thymus-homing bone marrow cells leads to intrathymic populations representing all four major Lyt-2- and L3T4-defined phenotypes. Although all four phenotypes may be represented in a single clone, quite often a striking bias in the proportion of L3T4 single positive to Lyt-2 single positive cells may exist within a clone, but not in the host thymocytes in general. Because at any one time these clones may be located in specific subregions of the thymus (specifically cortex only, medulla only, or cortex and medulla), we propose the hypothesis that different microenvironments in the thymus might, in fact, be responsible for the predominant maturation of different single positive mature thymic subsets.
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Thymus homing clonogenic bone marrow cells.
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Lymphocyte and lymphoma receptors utilized in differentiation, in homing, and in lymphomagenesis.
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Expression of major histocompatibility complex antigens in the thymuses of chimeric mice.
Thymuses of various types of bone-marrow-chimeric mice have been examined by tissue section immunologic staining for the presence and distribution of major histocompatibility complex (MHC) antigens. Cortical and medullary thymic epithelial cells continue to express thymus genotype I-A and H-2K/D antigens for at least 6 months posttransplantation. The appearance of bone-marrow-type MHC antigens is limited to low levels of H-2K/D on cortical and medullary lymphocytes, and to dendritic cells in the medulla; the medullary dendritic cells express high levels of donor-type I-A antigens as soon as 3 weeks posttransplantation. The observed patterns support the concept that I-A antigens are synthesized by thymic epithelial cells but are acquired by thymocytes. The findings are of relevance to the understanding of the role of the thymus in the generation of MHC restriction.
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Abnormal T-lymphocyte proliferation and cytotoxic responses induced by a neonatal injection of hydrocortisone: normalization by interleukin-2 addition.
Spleen cells from mice neonatally treated with hydrocortisone hemisuccinate (HHC) had an abnormal pattern of cell-mediated immunity when tested two weeks later. Mitogen-induced proliferation was reduced. The proliferative responses to allo-antigens were normal but the cytotoxic response thereby induced was impaired. The mechanisms of these anomalies are complex: reduction of cytotoxic precursors as measured by limiting dilution assays; enhancement of suppressor cells which are able to reduce the cytotoxic response of normal spleen cells; reduction of interleukin-2 (Il-2) production. The addition of exogenous Il-2 restores normal proliferative and cytotoxic responses.
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Modification of helper and suppressor/cytotoxic lymphocyte subsets in mice with motor end-plate disease.
Motor end-plate disease (Med) in mice is associated with complex immunological abnormalities which are shared by the heterozygous +/MedJ mice, which exhibit no or mild clinical manifestations, and by MedJ/MedJ mice which die from this neuromuscular disorder. In the present paper we extend our immunological data with the study of splenic lymphocyte subsets with Lyt monoclonal antibodies. Both MedJ/MedJ and +/MedJ 14-18 day old mice have high Lyt1+/Lyt2+ ratios, with higher Lyt1+ and reduced Lyt2+ lymphocyte pools as compared to normal mice. This correlates with the low suppressive function previously described, but is unexpected in view of the low helper function as measured by the response to SRBC immunization. Adult +/MedJ mice recovered normal T lymphocyte subset levels, while the small group of MedJ/MedJ mice that escapes death but continues to suffer from the neuromuscular illness maintains high Lyt1+/Lyt2+ ratios.
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Postnatal development of T cells. III. Thymus independency of T-cell-dependent antigen response in the neonatal spleen.
Neonatal spleens were grafted under the kidney capsule of adult syngeneic mice which were either normal, thymectomized, splenectomized or both thymectomized and splenectomized. After 14 days in situ, grafts were exised and the total cell number, the number of Thy-1 and Ig-positive cells, the plaque-forming cell (PFC) response after in vivo immunization with SRBC, and the suppressive activity in vitro on immune cells were determined. The expansion of the T-cell-precursor pool was not dependent upon the presence of the host thymus, nor was the antibody response, which was of neonatal type, i.e. with low PFC response and high suppressive activity. Host splenectomy enhances dramatically the proliferation of neonatal spleen graft cells and their ability to respond to SRBC. This enhancement is essentially due to a host cellular contribution, and is not observed when the graft is an adult spleen fragment. These results suggest that the spleen itself could have a regulatory role in postnatal lymphoid development.
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Impairment of T lymphocyte functions in mice with motor end-plate disease.
The present paper reports complex immunological anomalies associated with motor end-plate disease (Med) in mice. Motor end-plate disease is a severe neuromuscular disorder which leads to death (around the 25th of life) in the Medj/Medj mutant, while the heterozygotes quickly recover from mild manifestations. Medj/Medj and Medj/ + mice share some of the immunological aberrations: reduced PFC response to SRBC in 14-16 day old mice, with reduced suppressor cell function and precocious maturation of the cytotoxic response to allogeneic cells in 21-23 day old mice. The diminished PFC response is corrected in adult Medj/ + mice but persists in the small group of Medj/Medj which escape death and which were studied between the 6th and 16th week of life. In addition, the thymus and spleen of Medj/Medj mice are greatly reduced in size, a symptom which appears with the onset of the clinical disease. Also, a reduction in the NK activity in the small group of older, surviving mice was noted. T and B lymphocyte proportions and the proliferative responses to T cell mitogens were not impaired in 14-16 day old mice. The role of these abnormalities in the pathogenesis of the disease is not known. Since some of these anomalies are shared by Medj/Medj and Medj/ +, the latter of which present no or mild and transient neurological manifestations, there is no clear link between the immunological and neuromuscular disorders.
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Impairment of antibody response and of suppressor cell ontogenesis by early injection of hydrocortisone.
The appearance of antibody responsiveness against sheep red blood cells (SRBC) was studied in young mice treated with hydrocortisone hemisuccinate (HHC) either during gestation or around delivery (last 5 days of gestation or day of birth). The plaque forming cell (PFC) response was normal at 2 weeks and depressed at 4 weeks in animals treated during the last 10 days of pregnancy. Conversely, when HHC was only given around delivery, PFC response was depressed at 2 weeks and normal at 4 weeks. The presence of suppressor cells in unimmunized 1--2-week-old spleen cells was evaluated by co-culturing them with adult spleen cells from mice immunized against SRBC. Suppressive activity was found at high level at 8 days, and had already declined at 15 days in non-treated mice. Spleen cells from mice treated with HHC around delivery showed reduced suppressive activity at 8 days but this activity was very high on the 15th day, greater than in normal mice. Such highly suppressive activity correlated with a high level of Lyt-123 T cells. These data on suppressor cells indicate that the paradoxical effect of HHC in mice treated during gestation or around birth is probably explained by the differential effect of HHC on the kinetics of suppressor cells in ontogeny.
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Bone marrow cells give rise to distinct cell clones within the thymus.
The thymus is the major, if not the sole site of maturation of T lymphocytes from their haematopoietic precursors. During embryonic life (at a few well-defined intervals, at least in birds) the thymus receives thymus-homing haematopoietic precursors that give rise to antigen-specific functional T lymphocytes. Although the number and thymic location of distinct T-cell lineages destined to form the peripheral T-cell pool are not yet well defined, at least two independent pathways have been proposed. First, thymic subcapsular lymphoblasts divide and differentiate to give rise to small deep cortical thymic lymphocytes, medullary lymphocytes and thymus emigrants (I.W., unpublished data) and second, the medulla contains an independent self-renewing population that contains the precursors of the peripheral T-cell pool. Following irradiation the thymus may be repopulated by injected haematopoietic cells presumably related to the thymus-homing haematopoietic cells of the embryo. Here we have reconstituted irradiated mice with limiting numbers of bone marrow cells from Thy-1 congeneic donors and have found distinct clones of cells within the thymus. The pattern of reconstitution by the precursor cells indicates that two independent thymus lineages exist: cortex plus medulla, and medulla alone.
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