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Biomedical subjects

D Mason

Publications and source records attributed to D Mason.

At least 109 records · Page 6Linked to original sources
PubMed1993

Evidence that the T cell repertoire of normal rats contains cells with the potential to cause diabetes. Characterization of the CD4+ T cell subset that inhibits this autoimmune potential.

Diabetes was induced in a normal nonautoimmune rat strain by rendering the animals relatively T cell deficient using a protocol of adult thymectomy and sublethal gamma irradiation. All male rats and 70% of females developed an acute syndrome with severe loss of weight and hyperglycemia. Diabetes in these lymphopoenic rats was associated with extensive insulitis involving CD4+ and CD8+ T cells and macrophages. The CD8+ T cells were essential for the development of diabetes but not insulitis. The autoimmune diabetes and insulitis were completely prevented by the injection of a particular CD4+ T cell subset, isolated from healthy syngeneic donors, of the phenotype CD45RClow T cell receptor alpha/beta+ RT6+ Thy-1- OX-40-. Cells of this protective phenotype, which make up about 5% of thoracic duct lymphocytes, were found to provide help for secondary antibody responses and produce interleukin 2 (IL-2) and IL-4, but no interferon gamma, on in vitro activation. These data provide evidence for the presence of autoreactive T cells in the normal immune system of the rat and reveal that in the intact animal these cells are prevented from expressing their autoreactive potential by other T cells.

Animals↗
PubMed1993

Mike Grace talks to the President of the General Dental Council, Sir David Mason.

Dentistry, as with all things, moves in the direction of the thinking of those people within it, whether they are members of the dental team working within their surgeries, various colleagues in practice and on the many dental committees, teachers involved with undergraduates, people in the dental industry and trade, technicians in laboratories or leaders of the many organisations. This column will explore the thoughts and attitudes of many of these people--both those in the public limelight and those as yet unknown. To celebrate the launch of 'Interview with the Editor' who better to feature than the President of the General Dental Council, Sir David Mason. In this interview he shares his own thoughts and hopes for the future, thoughts that will influence the lives of most of the profession.

Education, Dental, Graduate↗
PubMed1993

Neighborhood nursing--the community as partner.

Neighborhood nursing seeks to make community health nursing activities more far reaching than those currently reimbursed by third parties, focusing on the issues of health promotion and disease prevention as significantly as the industry has focused on the acute care provision in home care. Yet variables in community nursing have changed what was the traditional focus of community health nursing practice. One agency is developing a program that will allow delivery of a different type of community health nursing. The outcome is a much richer delivery of care.

Community Health Nursing↗
PubMed1993

ICAM-3 expression on endothelium in lymphoid malignancy.

Intercellular adhesion molecule-3 (ICAM-3), the third receptor for lymphocyte function-associated antigen molecule-1 and a new member of the immunoglobulin superfamily has been recently characterized using specific monoclonal antibodies. In the present study, we show immunocytochemically that ICAM-3 is present on T and B cells in the mantle zones and on a subpopulation of follicular center cells in reactive lymph nodes and only occasionally in endothelium. In 52 cases of Hodgkin's disease, ICAM-3, although present on the majority of the reactive lymphoid cells, was absent from the Reed-Sternberg cells and their variants. However, in 28 cases (54%), there was prominent endothelial staining in small vessels. Similar findings were noted in 16 out of 49 cases (33%) of non-Hodgkin's lymphomas. This finding suggests that analogous to ICAM-1 and ICAM-2, ICAM-3 expression can be induced on endothelial cells in lymphoid neoplasms, probably by an as yet unidentified cytokine-mediated mechanism.

Antigens, CD↗
PubMed1992

Glucocorticoids induce the expression of CD8 alpha chains on concanavalin A-activated rat CD4+ T cells: induction is inhibited by rat recombinant interleukin 4.

Rat T lymphocytes, activated in vitro with concanavalin A (Con A), were shown by flow cytofluorographic analysis to contain a population of cells that simultaneously expressed CD4 and the alpha chain of CD8. The inclusion of the glucocorticoid hormone dexamethasone in the culture medium greatly increased both the frequency of these double-positive cells and the level of CD8 alpha chain expression. The level of expression of CD4 was not affected, and the cells that expressed CD8 antigen only also remained unchanged in surface phenotype. Detailed studies demonstrated unequivocally that the CD4+ CD8 alpha + cells were not artifacts produced by the random association of single-positive cells in the flow cytofluorograph, but arose from precursors that were single-positive CD4+ cells before activation. Furthermore, Con A activation of purified CD4+ T cells, in the presence of T cell-depleted accessory cells, showed that CD8+ T cells played no role in the induction process. However, the induction of CD8 alpha chain expression on CD4+ T cells and the enhancement of this expression by dexamethasone were almost completely inhibited by rat recombinant interleukin 4 (IL-4). Detection of mRNA for rat CD8 alpha chain by Northern blot closely paralleled the cell surface expression of CD8 alpha antigen, indicating that dexamethasone and IL-4 had opposing effects on mRNA levels. In contrast, IL-4 and dexamethasone both induced CD8 alpha chain expression on a rat CD4+ T cell clone when this was activated by specific antigen, and, although the effect with IL-4 was relatively weak, it did not antagonize the effect of the glucocorticoid. The possible significance of these results is briefly discussed.

Animals↗
PubMed1992

Monitoring progress toward US preschool immunization goals.

The United States has achieved over 97% immunization of children by school age and has reduced the incidence of vaccine-preventable diseases by more than 90% since the prevaccination era. However, children often do not receive immunizations at the recommended age, and in densely populated urban areas this delay in immunization has led to epidemics of measles. Correctable deficiencies of the immunization delivery system have been identified in these areas. To respond to needs, the public health infrastructure must be strengthened, and active participation from the private sector must be obtained, both in delivery of immunizations and in assessment of performance. Appropriate action must be stimulated by the provision of timely information on immunization coverage and on indicators of program performance at the local level.

Child, Preschool↗
PubMed1992

T-cell subsets in autoimmunity.

The demonstration that functionally different T-cell subsets can be defined by the isoforms of the leukocyte-common antigen, CD45, that they express, has prompted studies on the roles of these subsets in autoimmunity. The results have led to the identification of a particular subset of CD4+ T cells that have the ability to inhibit autoimmune disease. Further, it has been shown that diabetes in the B-B rat can be transferred by in vitro activation of T cells by Staphylococcal enterotoxin suggesting that superantigens may play a role in the pathogenesis of this disease. However, in this system too, it appears that a subset of T cells can inhibit the induction of autoaggressive cells. In other experimental autoimmune diseases there is evidence that CD8+ T cells can be protective and that these cells may mediate this protection by the synthesis of transforming growth factor-beta.

Animals↗
PubMed1992

Autoimmunity.

The immune system has evolved to protect an organism from the pathogens that invade it but the effector mechanisms involved in mediating this protection are potentially lethal to the host itself. Consequently it is essential that they are not elicited by the host's own tissues and, because biochemically self and non-self are very similar, the immune system has had to develop an exquisite capability to distinguish relatively minor differences. There has been considerable progress recently in understanding how this discrimination is achieved although many questions remain. The problem is important in that the mechanisms that ensure self tolerance occasionally fail. The consequences of this failure are the autoimmune diseases, many of which afflict Man. This article reviews what is known about the way that the immune system normally avoids self reactivity and how breakdown in self tolerance can occur.

Antigen-Presenting Cells↗
PubMed1991

Delayed exposure to pulsatile shear stress improves retention of human saphenous vein endothelial cells on seeded ePTFE grafts.

Since significant loss of endothelial cells (ECs) from the surface of a seeded prosthetic graft occurs after implantation, improved cell retention following exposure to flow should increase the likelihood of long-term success with this technology. An in vitro pulsatile flow circuit was developed to study the effects of two variables on cell retention: cell density at the time of seeding and postseeding incubation time. Fibronectin-coated ePTFE grafts (4 mm x 5 cm) were seeded with human saphenous vein ECs at two densities, confluent (1 x 10(5) cells/cm2) or subconfluent (2 x 10(4)), and incubated in vitro for varying time intervals (90 min, 1, 3, or 7 days). Test grafts were exposed to 90 min of pulsatile flow in an in vitro flow circuit, then fixed, and stained, and in situ cell counts (cells/cm2) were determined for nine representative fields per graft. Paired control grafts were treated identically but were not exposed to flow. Cell retention was calculated using the formula: % retention = cells/cm2 perfused graft divided by cells/cm2 control graft. Grafts exposed to flow 90 min after seeding demonstrated significantly lower cell retention when compared to later time points. When cells were seeded at confluent density, maximal retention (92 +/- 3%) occurred 24 hr after seeding. Prolonged culture of cells seeded on ePTFE grafts at confluent density resulted in increased cell loss. In contrast, on grafts seeded at subconfluent density, retention improved as cells grew to confluence (16 +/- 4.5% initially to 82 +/- 7% at 7 days).(ABSTRACT TRUNCATED AT 250 WORDS)

Blood Vessel Prosthesis↗
PubMed1991

Genetic variation in the stress response: susceptibility to experimental allergic encephalomyelitis and implications for human inflammatory disease.

Glucocorticoids that are released from the adrenal glands in response to stress can have profound effects on the immune system. Here, Don Mason illustrates how genetic variation in the magnitude of such a response can determine susceptibility to an experimental autoimmune disease in rats and discusses the implications for susceptibility to inflammatory diseases in humans. He also addresses the possible long-term effects of glucocorticoids on the balance between the cell-mediated and the humoral aspects of immunity and how this balance may influence the temporal development of an immune reaction.

Animals↗
PubMed1990

OX-22high CD4+ T cells induce wasting disease with multiple organ pathology: prevention by the OX-22low subset.

Congenitally athymic rats injected with CD45RBhigh CD4+ T cells from congenic euthymic donors developed a severe wasting disease with inflammatory infiltrates in liver, lung, stomach, thyroid, and pancreas. In contrast, recipients of CD45RBlow CD4+ T cells remained well and continued to gain weight. Animals given unfractionated CD4+ T cells, i.e., a mixture of approximately two-thirds CD45RBhigh and one-third CD45RBlow, were protected from the wasting disease, and the incidence of organ-specific inflammation was much reduced compared with that found in recipients of CD45RBhigh cells alone. The data suggest that this latter subset of CD4+ T cells has autoaggressive potential that is inhibited in normal animals by cells of the CD45RBlow CD4+ phenotype. The possible consequences of a breakdown in this immunoregulatory mechanism are briefly discussed.

Animals↗
PubMed1990

Fusion of influenza hemagglutinin-expressing fibroblasts with glycophorin-bearing liposomes: role of hemagglutinin surface density.

Influenza virus gains access to the cytoplasm of its host cell by means of a fusion event between viral and host cell membrane. Fusion is mediated by the envelope glycoprotein hemagglutinin (HA) and is triggered by low pH. To learn how many hemagglutinin trimers are necessary to cause membrane fusion, we have used two NIH 3T3 fibroblast cell lines that express HA protein at different surface densities. On the basis of quantitations of the number of HA trimers per cell and the relative surface areas of the two cell lines, the HAb-2 cells have a 1.9-fold higher plasma membrane surface density than the GP4F cells. The membrane lateral diffusion coefficient and the mobile fraction for HA is the same for both cell lines. A Scatchard analysis of the binding of glycophorin-bearing liposomes to the cells showed 1700 binding sites for the GP4F cells and 3750 binding sites for the HAb-2 cells, with effectively the same liposome-cell binding constant, about 7 x 10(10) M-1. Binding was specific for glycophorin on the liposomes and HA expressed on the cells. A competition experiment employing toxin-containing and empty liposomes allowed us to quantitate the number of liposomes that fused per cell, which was a small constant fraction of the number of bound liposomes. For the HAb-2 cells, about 1 in every 70 bound liposomes fused and for the GP4F cells about 1 in every 300 bound liposomes fused. Hence, the HAb-2 cells showed 4.4 times more fusion per bound liposome, even though the surface density of HA was only 1.9 times greater. We conclude the following: (i) One HA trimer is not sufficient to induce fusion. (ii) The HA bound to glycophorin is not the HA that induces fusion. That is, even though each HA has a binding and a fusion function, those functions are not performed by the same HA trimer.

Animals↗