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J E Balow

Publications and source records attributed to J E Balow.

157 records · Page 9Linked to original sources
PubMed1976

Human bone marrow lymphocytes. Cytotoxic effector cells in the bone marrow of normal individuals.

This study was undertaken to determine the capability of lymphocytes in the bone marrow of normal individuals to mediate nonspecific killer cell functions in assays of phytohemagglutinin (PHA)-induced cellular cytotoxicity, and antibody-dependent cellular cytotoxicity (ADCC) against 51Cr-labeled chicken erythrocyte target cells. Relatively pure mononuclear cell suspensions were obtained from bone marrow aspirates in 30 normal volunteers by sucrose gradient centrifugations and from the peripheral blood of the same individuals by Hypaque-Ficoll density centrifugations. At an effector: target ratio of 10:1, the PHA-induced cellular cytotoxicity of peripheral blood was 78.8 +/- 1.3%, while that of bone marrow was not significantly less at 66 +/- 9% (P greater than 0.1). At low effector:target ratios, the ADCC of bone marrow was negligible, while at higher effector:target ratios (20:1) bone marrow ADCC was 69 +/- 3.7%, which was comparable to that of peripheral blood. The lymphocytes themselves in the mononuclear cell suspensions of both peripheral blood and bone marrow were capable of cytotoxicity activity since depletion of monocytes from the suspensions by adherence to rayon wool and G-10 Sephadex columns did not remove the cytotoxic activity. Blocking of the Fc receptor on the effector cells by the addition of aggregated gamma globulin to the cultures suppressed the ADCC but not the PHA-induced cellular cytotoxicity of both peripheral blood and bone marrow, indicating that ADCC is dependent on an Fc receptor on the effector cell in both compartments. These studies demonstrate that the bone marrow of normal humans contains populations of lymphoid cells which have highly efficient killer cell capacities. It is uncertain what portion of these cells arise in the bone marrow and what portion enter the bone marrow parenchyma as part of the recirculating lymphocyte pool. These findings have relevance in the clearer understanding of the killer cell potential of grafted human marrow, as well as the bone marrow sequestration of functionally capable lymphocyte subpopulations in disease states and during chemotherapy.

Adult↗
PubMed1976

Glucocorticosteroid therapy: mechanisms of action and clinical considerations.

The administration of glucocorticosteroids results in a wide range of effects on inflammatory and immunologically mediated disease processes. Glucocorticosteroids cause neutrophilic leukocytosis together with eosinopenia, monocytopenia, and lymphocytopenia. A principal mechanism whereby corticosteroids suppress inflammation is their impeding the access of neutrophils and monocytes to an inflammatory site. Granulocyte function is relatively refractory, whereas monocyte-macrophage function seems to be particularly sensitive to corticosteroids. Corticosteroid administration causes a transient lymphocytopenia of all detectable lymphocyte subpopulations, particularly the recirculating thymus-derived lymphocyte. The mechanism of this lymphocytopenia is probably a redistribution of circulating cells to other body compartments. There is considerable disagreement about the direct effects of corticosteroid administration on human lymphocyte function. The corticosteroid regimen should be adjusted to attain maximal therapeutic benefit with minimal adverse side effects. Often, alternate-day dosage regimens effectively maintain disease remission with minimization or lack of Cushingoid and infectious complications.

Animals↗
PubMed1975

Experimental disseminated candidiasis. II. Administration of glucocorticosteroids, susceptibility to infection, and immunity.

A model of experimental disseminated candidiasis in inbred guinea pigs was used for study of the effects of both short-acting and long-acting glucocorticosteroid administration on the susceptibility to infection, the development of in vivo and in vitro parameters of cell-mediated immunity, and the expression of already established Candida-specific, cell-mediated immunity. Results revealed that long-acting glucocorticosteroids markedly potentiated infection, increasing mortality and suppressing already established cellular immune parameters. The development of cellular immunity to Candida was not impaired. Short-acting glucocorticosteroids, however, did not potentiate infection, and they affected neither the development nor the expression of immune parameters.

Animals↗
PubMed1975

Cyclophosphamide suppression of established cell-mediated immunity. Quantitative vs. qualitative changes in lymphocyte populations.

The characteristics of cyclophosphamide-induced suppression of established ccll mediated immunity were studied in guinea pigs previously senstized to tuberculin. Cyclophosphamide treatment for 5 days produced a dose-dependent peripheral lymphoctopenia and disproportionatley greater neutrophenia which was particularly striking at high doses of 20 mg/kg per day(approximaetly 200 mg/kg-2 per day). Lymphoctes remianing in the circulation of cyclophosphamide treeated aniamls showed a doses-dependent reduction to both in vitro proliferactive and macrophage migration inhibitory factor responses to tuberculin compared to lymphocte responses of controls. Proliferative responses to phytohemaggultinin and concanavalin a were not significatly suppressed. Additional studies showed that cyclophosphamide suppressed the porliferactive and migration inhibitroy factor responses to tuberculin of lymph node and splenic as well as cirulating lymphocte populations. These studies showed that relatively short-term cyclophospamide administration produced immunosuppresion by quantitative as well as qualitative changes in lymphocyte populations. Significant suppresion of lymphocte function, howerver, was achived only with doses of cyclophoshamide which also produced a severe neutropenia.

Animals↗
PubMed1975

Immunosuppressive effects of glucocorticosteroids: differential effects of acute vs chronic administration on cell-mediated immunity.

The effects of acute vs. chronic glucocorticosteroid administration on established cellular immune responses were studied in guinea pigs previously sensitized to tuberculin. A greater than 50% reduction in circulating lymphocytes was observed 4 hr after injection of soluble hydrocortisone and 24 hr after daily subcutaneous injections of depot cortisone acetate. After a single dose of hydrocortisone, peripheral lymphocyte migration inhibitory factor (MIF) production and antigen and mitogen-induced proliferation were unchanged. However, the peripheral lymphocytes remaining in the circulation after chronic cortisone treatment showed a marked decrease in both antigen-induced MIF and proliferation, although mitogen responses remained normal. Although similar levels of lymphocytopenia were induced by acute and chronic glucocorticosteroid administration, only chronic treatment was associated with depression of certain cell-mediated lymphocyte functions. The available evidence suggests that these changes may depend on GCS-induced selective alterations in the circulation patterns of certain subpopulations of lymphocytes.

Animals↗
PubMed1973

Glucocorticoid suppression of macrophage migration inhibitory factor.

The ability of hydrocortisone to modify antigen-mediated inhibition of macrophage migration, an in vitro correlate of cellular immunity in the guinea pig, was investigated. Only the glucocorticoids, hydrocortisone and dexamethasone, significantly blocked migration inhibitory factor (MIF) activity in pharmacologic concentrations. Hydrocortisone had no effect on antigen "processing" by macrophages, nor on the ability of antigen-stimulated peritoneal exudate lymphocytes to produce MIF. Rather, hydrocortisone antagonized directly the inhibitory effect of MIF on the macrophage.

Ascitic Fluid↗
PubMedDate not supplied

Glucocorticosteroid action on the immune system: molecular and cellular aspects.

The history of glucocorticosteroid therapy and modern rheumatology are inseparable. Glucocorticosteroids exert profound effects on the inflammatory and immune responses. They affect the growth, differentiation and function of monocytes and lymphocytes, the distribution of cellular subsets, and the production of cytokines. Glucocorticosteroid-induced lipocortins inhibit eicosanoid production and release by suppressing phospholipase A2. The principal mechanism whereby they exert their powerful effects is through modulation of the transcription of specific sets of genes. Recently, post-transcriptional mechanisms have also been recognized to be affected by glucocorticosteroids. In this review we discuss the molecular and cellular aspects of glucocorticosteroid action on the immune system.

Glucocorticoids↗
PubMedDate not supplied

Immunoglobulin deficiency in patients with systemic lupus erythematosus.

Hypergammaglobulinemia is a common laboratory finding in patients with active systemic lupus erythematosus; in contrast, immunoglobulin deficiency, except for immunoglobulin A, is unusual. We report 18 patients who developed low immunoglobulin G levels 4 months to 22 years (median = 4 years) following the diagnosis of systemic lupus erythematosus. This phenomenon was transient in 10 patients (median duration 10.5 months). Eight patients had received cytotoxic drugs prior to the development of hypogammaglobulinemia, while all had received prednisone. The nadir levels of serum IgG were 132-550 mg/dl (median = 363 mg/dl). The presence and degree of immunoglobulin G deficiency did not correlate, in general, with the type or dose of medication. None of the patients had renal failure. Only 4 patients developed recurrent infections. Urinary loss of protein was not a cause of this disorder. Study of the in vitro cellular immune responses of peripheral blood lymphocytes in 5 patients showed that excessive 'suppressor' T cell activity and decreased numbers of B cells may be responsible for the development of immunoglobulin deficiency. Serum immunoglobulin levels should not be employed as an indication of disease activity in systemic lupus erythematosus, as all 18 patients continued to have significant clinical disease. Deficiencies of immunoglobulins are often transient and may not require treatment.

Adolescent↗
PubMedDate not supplied

The nephropathy of systemic lupus erythematosus.

Lupus nephritis may be considered the prototypic autoimmune disease which is initiated by immune complex deposition. Several patterns of localization of immunoreactants are observed in lupus nephritis, but few data are available to elucidate the corresponding immunopathogenetic mechanisms. Corticosteroids form the mainstay of therapy for lupus nephritis, provided that they achieve a prompt clinical remission which can be sustained with alternate day therapy. Cyclophosphamide may have fewer risks than extended high-dose prednisone and it has been shown to be more efficacious than corticosteroids in preventing end stage renal failure.

Azathioprine↗
PubMedDate not supplied

Activated T lymphocytes in the peripheral blood of patients with systemic lupus erythematosus induce B cells to produce immunoglobulin.

Systemic lupus erythematosus (SLE) is characterized by multiple T and B cell abnormalities. This study was designed to investigate the cell surface membrane characteristics of T cells by using single and double immunofluorescence and examine the role of HLA-DR+ T cells in the production of immunoglobulin by B cells. The results presented: (a) confirm the presence of a larger population of T-cells bearing DR antigens in patients with SLE than in normal controls, (b) demonstrate that DR positive cells are equally distributed in helper/inducer and suppressor/cytotoxic subsets of lymphocytes from patients with SLE, (c) show no elevation in the percentage of T cells bearing interleukin 2 (IL-2) receptors, (d) demonstrate that DR positive, but not DR negative T-cells, multiply in the presence of conditioned media and, (e) demonstrate that DR positive T cells provide helper factors which enhance the production of immunoglobulin by B cells. We propose that T-cells bearing DR antigens in patients with SLE are functional in vivo, and may be responsible for the B cell overactivity.

Antigens, Surface↗