PubMed HealthSearch

SEARCH · PubMed Health

Results for “Lymphocyte Depletion”

Explore indexed PubMed citations for clinical trials, systematic reviews and public health research. Read source abstracts and follow each citation to its original PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 19 recordsLinked to original sources

Pulmonary vascular response to endotoxin in normal and lymphocyte depleted sheep.

The cardiopulmonary effects of intravenously administered Escherichia coli endotoxin were studied in unanesthetized sheep. One group of animals was depleted of circulating T-lymphocytes while a non-depleted group served as control. T-lymphocyte depletion was accomplished by chronic thoracic duct drainage of lymph, removal of lymphocytes by continuous flow centrifugation and return of the cell free lymph intravenously. The T-lymphocyte depleted sheep demonstrated markedly obtunded increases in pulmonary arterial pressure and pulmonary vascular resistance following endotoxin when compared to the effects of the lipopolysaccharide in control animals. additionally, the lymphocyte depleted group showed a significant augmentation of myocardial contractility which occurred at the same time as marked systemic hypotension. This period of extreme hypotension following endotoxin is presumed to be accompanied by a reflex increase in the activity of the sympathetic nervous system. The control sheep, although equally hypotensive at this time, did not demonstrate a significant increase in myocardial contractility from the preendotoxin value. The results of these experiments indicate that T-lymphocytes may mediate some of the pathophysiological effects of bacterial endotoxin on the cardiovascular system.

Animals

Lymphocyte depletion induced by cholera toxin; relationship to adrenal cortical function.

Intravenous injection of cholera toxin (choleragen) into mice caused a profound lymphocytopenia associated with marked cellular depletion of the lymph nodes, spleen, and thymus. After administration of 1 mu g of choleragen, lymphocytopenia was mot marked at 24 hr; recovery occurred 6 to 10 days later. Similarly depletion of lymph nodes and spleen was maximal at 24 hr with recovery by 14 days. Choleragen also caused a marked elevation of serum corticosterone and lymphocyte depletion was not observed in adrenalectomized mice. These results suggested that the lymphocytopenic effect of choleragen was mediated by increased production and secretion of adrenal cortical hormones secondary to a rise in intracellular cAMP induced by cholera toxin. The site of action of choleragen may be the adrenal cortex itself and/or the hypothalamic-pituitary system.

Adrenal Cortex

Experimental murine candidiasis: pathological and immune responses in T-lymphocyte-depleted mice.

Mice depleted of T-lymphocytes by thymectomy and irradiation (TXB) and immunologically competent mice were compared for gross and histological pathology as well as immune responses after cutaneous and/or intravenous challenge with Candida albicans. In response to a first cutaneous inoculation with viable Candida, TXB, sham-operated (SXB), and unmanipulated (normal) mice, all developed lesions of comparable size, duration, and histopathology. When challenged a second time cutaneously, normal and SXB mice developed lesions which were greatly increased in size when compared with those produced by a first cutaneous infection, whereas TXB mice developed lesions comparable in size to those initiated by the first infection. Histologically, the first and second lesions in all animals were acute abscesses predominantly comprised of polymorphonuclear leukocytes. The larger second lesions in SXB and normal mice were accompanied by detectable circulating antibody and by delayed hypersensitivity. Neither circulating antibody nor delayed hypersensitivity were stimulated in the TXB mice. When challenged intravenously, all previously uninfected mice, regardless of T-cell status, were equally susceptible to C. albicans. Contrary to SXB or normal mice, however, TXB mice which had been infected cutaneously were not more resistant to a subsequent intravenous challenge as judged by 6-week survival. The results suggest that T-cells do not play a significant role in innate resistance of mice to systemic candidiasis, but that such cells are important in the development of acquired resistance.

Antibodies, Fungal

Lack of B lymphocyte depletion from murine spleen cell populations by a human gamma-globulin, anti-human gamma-globulin column system.

It has been reported previously that enriched populations of mouse thymus-dependent (T) lymphocytes could be prepared by the use of a column procedure that is believed to remove selectively cells with receptors for antigen-antibody complexes. In our hands, this procedure does not selectively remove B lymphocytes but rather masks the surface immunoglobulin. Analysis of the column-passed cells revealed an apparent decrease in the percentage of immunoglobulin-bearing cells but little decrease in either the percentage of complement receptor lymphocytes or the mitogenic response to lipopolysaccharide. Furthermore, rabbit immunoglobulin could be detected on the surface of 35 to 45% of the cells emerging from the columns prepared with rabbit anti-human gamma-globulin (HGG). After overnight incubation, 30 to 40% of the emerging cells reexpressed mouse immunoglobulin on their surfaces. Adsorption of the antisera used to make the columns with mouse gamma-globulin (MGG) diminished the depleting capacity of the columns. We conclude from these observations that antibodies in the anti-HGG sera, cross-reactive with mouse immunoglobulin, account for the spacious depletion of B lymphocytes observed when cells are passed over these antigen-antibody complex columns.

Animals

Immune responses to organ allografts. II. Decreased B cell responses to cardiac allografts in rats pretreated with enhancing, suppressor cell, or T lymphocyte depletion protocols.

Primarily vascularized LBN cardiac allografts transplanted to LEW rats are rejected 6 to 8 days after transplantation. Immunoperoxidase stains for cells producing immunoglobulin (Ig) demonstrate a proliferation of Ig-containing immunoblasts in the splenic red pulp (RP) and peripheral periarterial sheath (PAS) within 2 days after transplantation. These immunoblasts differentiate into plasma cells that triple the RP volume by the time of rejection. By 14 days, the plasma cells are replaced by mitotically active large and small lymphocytes with no demonstrable cytoplasmic Ig. Splenic Ig production is followed by a venous vasculitis in the graft and by the appearance of circulating cytotoxic antibodies 5 days after grafting. Three biological methods of prolonging cardiac graft survival were found to derange this sequence of immunological reactions at different stages. Enhancement by antigen and antibody pretreatment of the recipient elicited a premature production of Ig that subsided and was not reinitiated by cardiac transplantation. Transfer of suppression with thymocytes from enhanced cardiac recipients temporarily inhibited differentiation of splenic B cells into immunoblasts and plasma cells. T cell depletion by thymectomy, irradiation, and bone marrow reconstitution also decreased the plasma cell response, possibly by removing helper cells required to switch IgM production to IgG. These studies reemphasize the importance of Ig production in the complex interaction of immune reactions leading to acute rejection of organ transplants.

Animals

[Immune response and tolerance to S. typhi Vi-antigen in T-lymphocyte depleted mice].

Comparison of immune response to Vi-antigen in thymetomized letally irradiated and reconstituted with fetal liver cells mice and in control animals revealed no difference between the two groups. The absence of enchancement of antibody formation in T cell depleted mice favours thymic-independent regulation of immune response to optimal dose of Vi-antigen. The induction of cyclophosphamide tolerance to Vi-antigen did not depend on the presence of T cells: tolerogenic treatment was equally effective in T cell depleted mice and in control animals. Therefore cyclophosphamide tolerance was not due to the activation of T suppressors but to direct elimination of immunocompetent clones of B cells.

Animals

The significance of urinary melanoma antigen excretion and the ability of thymosin to raise the level of depleted lymphocytes in vitro in malignant melanoma.

One hundred and fifty-six patients were screened for the presence of urinary melanoma antigen and serum cytoplasmic antibody. It was found that 44% of symptomless Stage 1 patients tested five to 15 years after operation had detectable antigen (Ag) in their urine; the urines of 67% of Stage 2A (local recurrence) patients were positive for Ag; while in only 38% of those patients graded 2B (lymph-node involvement) were these tests positive. Urines of 83% of patients with generalized metastases (Stage 3) were positive. A sequential study was made of 23 patients seen and treated in 1976. Of this group, 14 reverted from a positive state to a negative one following excision of their tumour, while six were negative on first postoperative testing and subsequently became positive. Three out of the 23 remained persistently negative. T lymphocyte levels were assessed in 71 melanoma patients, and a stage-related fall was noticed. Thymosin (Hoffman LaRoche) on in vitro incubation significantly raised the levels of T lymphocytes.

Adult

The localization of Hodgkin's disease in lymph nodes. A study with immunohistological, enzyme histochemical and rosetting techniques on frozen sections.

Lymphoid tissue of 51 patients with Hodgkin's disease was studied with immunohistological, enzyme histochemical and rosetting techniques for the detection of B and T cells in frozen sections. In lymph nodes of patients with lymphocyte predominance type of Hodgkin's disease, the majority of the lymphocytes in the involved areas were normal B lymphocytes of polyclonal origin. This was also true for nodular sclerosis cases with a predominance of lymphocytes. Surrounding Sternberg-Reed cells small clusters of T lymphocytes could be demonstrated. In mixed cellularity and also in nodular sclerosis with a mixed cellular pattern only small residual areas of B lymphocytes were present, whereas relatively large numbers of T lymphocytes were found in the involved areas. In lymphocyte depletion B lymphocytes were scarce and T lymphocytes were present in small number. It is concluded that different patterns of lymphocyte population can be discerned in the subtypes of Hodgkin's disease. A predominance of B lymphocytes is found in cases with lymphocyte predominance and thus is a prognostic favourable sign. A predominance of T lymphocytes as found in cases with a mixed cellular pattern with or without nodular sclerosis is therefore not a favourable sign in general but may indicate progressive disease. The possible reasons for the presence of large numbers of B or T lymphocytes in lymphoid tissue affected by Hodgkin's disease are discussed.

B-Lymphocytes

Architectural alteration of lymphatic tissue produced by extracorporeal thoracic duct filtration.

Removal of recirculating lymphocytes from the lymph of calves by extracorporeal thoracic duct filtration results in a state of immunounresponsiveness. Accompanying this is histological evidence of lymphocyte depletion from the lymph organs and structures of the body. Lymph nodes, spleen, hemolymph nodes, Peyer's patches, and thymus appear depleted of the recirculating small lymphocyte. We find this closed model of lymphocyte depletion effective and free of seyere problems with infections and physiological alterations as experienced in mechanical removal, extracorporeal irradiation, and open thoracic duct fistulas.

Animals

Antibodies to Epstein-Barr virus-associated nuclear antigen and to other viral and non-viral antigens in Hodgkin's disease.

Antibody reactivity to Epstein-Barr virus (EBV)-associated nuclear antigen (EBNA) was investigated by means of the anticomplement immunofluorescence technique on sera from patients with Hodgkin's disease (HD) and from appropriate controls. Antibody levels to other EBV-determined antigens, i.e. viral capsid (VCA) and early antigens (EA), and to measles and rubella viruses, to cytomegalovirus (CMV), and to toxoplasma gondii were also measured. The results of anti-EBV antibody titrations demonstrated that anti-VCA, anti-EA and anti-EBNA reactivity was significantly higher in HD patients than in healthy subjects. There was no significant difference between the distribution of high rubella and measles antibody titers in HD and control sera. The GMT and the incidence of high titer anti-CMV and toxoplasma antibodies were greater in HD patients than in controls. The analysis of the data, according to histological subtypes, showed that the condition of lymphocyte depletion was associated in HD patients with the highest anti-EBNA antibody levels and the lymphocyte predominance with the lowest. This pattern seemed to be peculiar for anti-EBV reactivity, since anti-CMV and anti-toxoplasma antibody levels in the lymphocyte-depleted group of patients did not significantly differ from those of controls. No correlation was found between anti-VCA and anti-EBNA in individual sera of HD patients. This observation suggests that different mechanisms are probably responsible in HD for the release of EBV-related antigen from infected cells.

Adolescent

Epstein-Barr virus interactions with human lymphocyte subpopulations: virus adsorption, kinetics of expression of Epstein-Barr virus-associated nuclear antigen, and lymphocyte transformation.

In order to further understand Epstein-Barr virus (EBV)-lymphocyte interactions, we investigated a chain of events including: (i) EBV binding to human lymphocyte subpopulations; (ii) the earliest appearance of EBV-determined nuclear antigen (EBNA) in the lymphocytes after EBV infection; and (iii) establishment of continuous lymphoblastoid cell lines (LCL) by infecting with EBV different types of lymphocyte preparations from the same as well as from different donors. By using direct membrane immunofluorescence assay, we found that only a small fraction of human peripheral blood and cord blood lymphocytes (CBL), and possibly less than 31% of the T cell-depleted lymphocyte population, carry receptors for P3HR-1 strain of EBV. The number of cells carrying receptors for EBV did not vary considerably among different blood lymphocyte populations from several normal donors. EBV adsorption on lymphocyte subpopulations showed that purified thymus-dependent (T) cells and thymocytes did not adsorb EBV, in contrast to T cell-depleted lymphocyte populations and lymphoid cells from fetal liver and spleen. In CBL infected with EBV strain B95-8, EBNA was detected by anti-complement immunofluorescence as early as 18 h after infection. This indicates that EBNA is the earliest detectable EBV-determined intracellular antigen to appear after infection and before or during lymphocyte transformation by EBV. Transformation was observed only in lymphocyte cultures containing detectable thymus-independent B cells but not in cultures of purified T cells. With one exception (es-b-1), all the EBV-transformed LCL from different origins carried surface-bound immunoglobulins (a B cell marker). These included also the 10 LCL obtained by infecting cultures of adherent cells from different donors. With regard to its surface markers, ES-B-1 appeared to be an exceptional EBV genome-carrying line, and it also lacked the ability to form spontaneous rosettes with sheep erythrocytes (a T cell marker). Therefore, it is possible that ES-B-1 was derived from an atypical B cell or B cell precursor or from a so-called "null cell" transformed by EBV.

Adsorption

Post-capillary venules of the mouse lymphatic tissues with special reference to the distribution of their endothelial IgG.

Post-capillary venules (PCV) of the lymph nodes and Peyer's patches were studied in frozen sections stained with an indirect immunoperoxidase technique to demonstrate their endothelium-associated IgG in DBA/2 mice rendered T-lymphocyte depleted with anti-theta- and anti-thymus-globulins. Three types of IgG-distribution (luminal, intraendothelial and basement membrane, types I, II and III, respectively), each confined to one of the three PCV grades (graded on the basis of the endothelial cell height), could be distinguished. The PCV grades, on the other hand, were closely correlated with the degree of T-lymphocyte depletion. The significance of this intimate relationship between the IgG-distribution pattern and the PVC grades was discussed in regard to the T-lymphocyte recirculation. A hypothesis was presented describing the presumed sequence of events involved in the passage of T-lymphocytes through the endothelium of the PCV which is the crucial step in their recirculation from blood of the lymphatic tissue.

Animals

Dicarbocyanine fluorescent probes of membrane potential block lymphocyte capping, deplete cellular ATP and inhibit respiration of isolated mitochondria.

3,3'-Dipropylthiodicarbocyanine iodide, a widely used fluorescent probe of membrane potential, was found to inhibit anti-Ig antibody, induced capping of mouse lymphocytes. The dye also lowered the cell ATP content. Experiments with isolated mitochondria revealed that the probe had a potent inhibitory action at site I of the respiratory chain. This mitochondrial blockade helps to explain the ATP depletion and blockade of capping, and gives cause for caution in the use of this dye as a probe of cell membrane potential. Three related dicarbocyanine dyes had similar toxic effects, but two cyanine dyes with much longer alkyl side chains, which have been used as probes of membrane fluidity, did not.

Adenosine Triphosphate