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Biomedical subjects

A R Rabson

Publications and source records attributed to A R Rabson.

At least 55 records · Page 3Linked to original sources
PubMed1984

Prevention of antisperm autoantibody response in vasectomised Swiss white mice by infusion of heterologous antisperm serum.

Antisperm autoimmunisation may cause infertility in men following spermatic cord torsion, testicular biopsy and vasectomy with attempted reversal. The demonstration in addition of antisperm autoantibody-associated systemic disease in animals is cause for concern, although there is to date little evidence for these effects in man. We have investigated the use of heterologous antisperm antiserum to block the autoimmunising effect of vasectomy in Swiss white mice. Antisperm autoantibodies were detected by microimmunofluorescence at 1/8 dilution in all eight control mice tested 1 month after vasectomy, and in none of the five mice who had received high-titre or low-titre immune serum (P less than 0.001). However, the high-titre serum was toxic in the amounts used.

Animals↗
PubMed1984

Prostaglandin E2 depresses natural cytotoxicity by inhibiting interleukin-1 production by large granular lymphocytes.

Enriched large granular lymphocytes treated with varying concentrations of prostaglandin E2 (PGE2) for varying time periods showed considerably reduced natural cytotoxicity against K-562 target cells. The same cells when activated by lipopolysaccharide, produced substantially less interleukin-1 (IL-1) as compared to cells not treated with PGE2. It is concluded that the inhibition of natural killer (NK) cell activity produced by PGE2 is due to inhibition of IL-1 production by these cells.

Cell Line↗
PubMed1983

Supernatant derived from a human hepatocellular carcinoma cell line (PLC/PRF/5) activates a population of T-suppressor cells.

Harvest fluid derived from a primary hepatocellular carcinoma cell line (PLC/PRF/5) inhibited the incorporation of 3H-thymidine into PHA-activated human lymphocytes. A similar effect was observed when lymphocytes were pre-incubated with the tumour supernatant and washed prior to mitogen activation. Not only did the tumour supernatant inhibit 3H-thymidine incorporation by mitogen-activated lymphocytes, but it also inhibited production of the lymphokine leucocyte inhibitory factor (LIF). In experiments designed to establish whether a component of the tumour harvest fluid was activating a population of suppressor cells, normal mononuclear (MN) cells were treated with the PLC/PRF/5 or embryonic fibroblast supernatant for 48 h, after which they were washed and added to normal mitogen-activated lymphocyte cultures. Only cells pretreated with the PLC/PRF/5 supernatant suppressed mitogenesis. The cell responsible for the suppressor effect was a T cell, which after a further 24 h in culture liberated a suppressor factor responsible for inhibiting lymphocyte function. Although the nature of the factor/s in the PLC/PRF/5 supernatant responsible for activation of the T-suppressor cell population is unknown, it is suggested that this mechanism may be important in protecting the tumour from the immune response.

Animals↗
PubMed1983

Supernatant derived from a human hepatocellular carcinoma cell line (PLC/PRF/5) depresses natural killer (NK) cell activity.

Harvest fluid derived from a human primary hepatocellular carcinoma cell line (PLC/PRF/5) inhibited normal peripheral blood NK-cell activity when either PLC/PRF/5 or K562 cells were employed as targets. MN cells incubated with the PLC/PRF/5 supernatant for only 6 h demonstrated depressed NK-cell activity, which was partially reversible if the cells were washed and incubated in fresh medium for 24 h. Enriched NK cells obtained on discontinuous Percoll gradients employing human tonsillar cells also showed depressed cytotoxicity when treated directly with the tumour harvest fluid. Furthermore, the binding of these cells to the tumour targets could be inhibited by prior treatment of the NK cells with the tumour supernatant. It is suggested that materials produced by tumours may inhibit NK-cell activity by blocking a receptor site on the effector cell, thereby allowing the tumour to proliferate.

Animals↗
PubMed1983

The effect of hydrocortisone (HC) on sodium periodate and phytohemagglutinin-induced [3H]thymidine incorporation and lymphokine production by human lymphocytes.

Hydrocortisone (HC) in pharmacologically attainable concentrations was shown to inhibit mitogen-induced lymphocyte blastogenesis. When adherent and nonadherent cells were treated separately with hydrocortisone and then reconstituted, treatment of either cell population resulted in a diminished mitogen-activated response. HC-treated adherent cells produced less interleukin 1 (IL-1) than control cells, and interleukin 2 (IL-2) production by HC-treated lymphocytes was also reduced. This latter finding could not be reversed by adding IL-1-containing adherent cell supernatants to the culture systems. Leukocyte inhibiting factor (LIF) production by sodium periodate-activated mononuclear cells was also reduced after HC treatment, but could be corrected by adding IL-1-containing adherent cell supernatants to the cultures. PHA-induced LIF production, which is less dependent upon adherent cells and their products, was not affected by HC treatment. It is concluded that HC exerts its suppressive effect by independently inhibiting IL-1 production by adherent cells and IL-2 production by lymphocytes.

Animals↗
PubMed1983

Mononuclear cell function in Mycobacterium tuberculosis infected guinea pigs.

In this study mononuclear cell function was studied in the lymph glands, spleen, and peripheral blood of Mycobacterium tuberculosis infected guinea pigs. Adherent cells from draining lymph nodes and spleens of infected animals spontaneously produced a factor which inhibited normal lymphocyte proliferative responses. As it has previously been shown that this factor activates a population of suppressor T cells, resident lymphocytes in the lymph nodes and spleen were examined and were shown to inhibit normal lymphocyte functions. It is suggested that adherent cells ingesting M. tuberculosis spontaneously release a suppressor cell activating factor (SCAF) which locally activates lymphocytes to become suppressor cells. Even at a time of overwhelming infection, peripheral blood adherent cells could not be shown to release SCAF and peripheral blood suppressor cells could not be identified. Although peripheral blood lymphocyte proliferative responses to PHA were normal in infected animals, their ability to produce the lymphokine macrophage inhibition factor was considerably reduced after the second week of infection. This dissociation between lymphocyte proliferation and lymphokine production is similar to that previously described in humans overwhelming tuberculosis.

Animals↗
PubMed1983

Lymphocyte subsets in measles. Depressed helper/inducer subpopulation reversed by in vitro treatment with levamisole and ascorbic acid.

Lymphocyte subsets were assessed in patients with measles using the OKT range of monoclonal antibodies. A significant decrease in cells reacting with the OKT3 and OKT4 monoclonal antibodies was observed. When the tests were repeated 3 wk after the acute infection, significant recovery of these subsets was observed. The abnormality in lymphocyte subsets could be reproduced by treating normal lymphocytes with measles virus in vitro. When lymphocytes from patients with measles or when normal cells infected with measles virus in vitro were treated with either levamisole or L-ascorbic acid for 15 min and then retested with the OKT antisera, restoration of the previously depleted OKT3+ and OKT4+ cell population was observed. Ascorbic-acid treatment also, to a certain extent, reversed the inability of measles mononuclear cells to produce lymphocyte mitogenic factor (helper factor for B cells) after pokeweed mitogen activation. This abnormality, however, could not be reversed by in vitro treatment with levamisole. Measles patients treated with L-ascorbic acid demonstrated no accelerated recovery in either their lymphocyte subset profile or their ability to produce lymphocyte mitogenic factor. Although the cause of the depressed OKT3+ and OKT4+ lymphocyte subpopulations in patients with measles is not clear, the results suggest that the effect is not due to an aberration of protein synthesis, but rather to a blocking or steric change produced by the virus on the cell membrane. It is likely that both ascorbic acid and levamisole have the ability to reverse this effect by virtue of their antioxidant properties.

Acute Disease↗
PubMed1983

Characterization of a suppressor cell-activating factor (SCAF) released by adherent cells treated with M. tuberculosis.

Peripheral blood adherent cells ingesting killed Mycobacterium tuberculosis release a suppressor cell-activating factor (SCAF) into their culture supernatants. When adherent cells ingested 125I-labeled M. tuberculosis, radioactivity could be detected in the supernatant within 2 hr. When this supernatant was fractionated on a Sepharose 2B column, the fraction with suppressor cell-activating activity was also found to contain the majority of the radiolabel, which suggests that the macrophage processed bacteria (or bacterial product) constituted the major portion of the SCAF. This fraction also contained a high proportion of lipid, and the fraction with suppressor activity resided purely within the phospholipid fraction. By employing thin layer chromatography, the phospholipids responsible were identified as phosphatidylethanolamine and phosphatidylinositol. These results indicate that when macrophages ingest mycobacteria, they release phosphatidylethanolamine and phosphatidylinositol of bacterial origin into their culture supernatants, which are responsible for activating suppressor T cells.

Cell Adhesion↗
PubMed1983

Binding of phosphatidylethanolamine and phosphatidylinositol to OKT8+ lymphocytes activates suppressor cell activity.

The phospholipids phosphatidylethanolamine (PE) and phosphatidylinositol (PI) have been shown to activate a population of OKT8-enriched lymphocytes to become activated suppressor cells that result in the suppression of lymphocyte blastogenesis to a variety of mitogens and antigens. This suppression is dose dependent, and maximal suppressor activity is obtained at concentrations of 125 micrograms/ml PE and 25 micrograms/ml PI. Activation of the suppressor cell population is not associated with an actual increase in the number of cells expressing the OKT8 antigen, but the number of these cells expressing Dr antigens on their surface was increased. Both PE and PI bound to lymphocytes in a specific manner. Binding of radiolabeled PE could be inhibited by unlabeled PE but not by PI or phosphatidylserine (PS). Similarly, the binding of PI to lymphocytes was also found to be specific. Although radiolabeled PE bound to lymphocytes other than OKT8+ cells, and to other peripheral leukocytes, it bound to OKT8+ cells with a significantly greater affinity than it did to the other cell types. The Kd for PE was 1 x 10(2) nM and for PI was 1 x 10(3) nM, and receptor cell densities for these two phospholipids were estimated at 1 x 10(-8) nM and 3 x 10(-9) nM, respectively. The receptors for these two phospholipids were trypsin and heat sensitive, and the receptor sites could be regenerated after a 24-hr incubation after trypsinization.

Antibodies, Monoclonal↗
PubMed1983

Lymphocyte subtypes in patients with atopic eczema, protein calorie malnutrition, SLE and liver disease.

Peripheral blood lymphocytes from patients with protein calorie malnutrition, atopic eczema, systemic lupus erythematosus and in three groups of patients with liver disease, were characterized by reactivity with monoclonal antibodies to the surface antigens of helper-inducer (OKT4) and suppressor-cytotoxic (OKT8) T cell subsets and to a common T cell antigen (OKT3). The protein calorie malnutrition group showed a considerable decrease in all subsets while patients with atopic eczema displayed an increase in the total number of OKT3+ cells, attributable primarily to an increase in the OKT4+ cell population with the OKT8+ cells remaining within normal values. In the SLE group, only 3 of the 16 patients had OKT8+ numbers below that of normal controls, whereas the mean number of OKT4+ cells in the group was less than normal controls. The striking feature of patients with liver disease, was the altered ratio of OKT4+ to OKT8+ cells in the hepatocellular carcinoma and amebic liver abscess groups due primarily to decreased OKT4+ and raised OKT8+ cell subpopulations.

Antibodies, Monoclonal↗
PubMed1983

The effect of interleukin 1(IL-1) containing supernatants on murine thymocyte maturation.

IL-1 containing supernatants were produced by E. coli lipopolysaccharide (LPS) stimulated adherent human mononuclear cells. Thymocytes from 4--6-week-old BALB/c mice were pretreated with IL-1 containing supernatants or control supernatants. IL-1 containing supernatant pretreated thymocytes when added to enriched splenic B cells increased the proliferative response of these cells after PWM activation. IL-1 pretreated thymocytes furthermore, increased the number of immunoglobulin secreting cells in the mouse splenocyte population, as compared to control supernatant pretreated thymocytes. These results indicate that IL-1 matures thymocytes into predominantly helper cells which augment B cell proliferation and antibody production.

Animals↗
PubMed1982

Depressed natural killer cell activity in patients with hepatocellular carcinoma. In vitro effects of interferon and levamisole.

Enriched lymphocytes from patients with primary hepatocellular carcinoma showed considerably reduced natural cytotoxicity against two established hepatoma cell lines and against the myelogenous derived cell line K562, as compared to lymphocytes from normal volunteers or from patients with various nonmalignant liver diseases. The serum of hepatoma patients did not effect normal or patient NK cell activity. When lymphocytes from patients or controls were treated for three hours with human leukocyte interferon, NK cell cell activity was significantly improved. Levamisole did not produce a significant increase in normal NK cytotoxicity but did improve the killing of lymphocytes from patients with hepatocellular carcinoma.

Adult↗
PubMed1982

A case of Di George syndrome treated with thymopoietin pentapeptide (TP-5) demonstrating an adherent suppressor cell of lymphocyte function.

A child with the classical features of Di George syndrome is described. The patient was treated with TP-5 and the number of peripheral blood E-rosette forming cells rose from 11% to 69% but then fell to 33% prior to death. There was poor correlation between the number of T-cells estimated by rosetting with sheep red blood cells and that measured by cytotoxicity to the OKT3 antiserum and complement. Although the total T-cell numbers were reduced, the ratio of inducer/helper cells: suppressor/cytotoxic cells remained normal as assessed by the use of the specific monoclonal antisera OKT4 and OKT8. Lymphocyte proliferation after mitogenic activation and the production of lymphocyte mitogenic factor by PWM stimulated lymphocytes was significantly depressed but was considerably improved by the removal of adherent cells. It appears as though an adherent suppressor cell was partially responsible for the depressed lymphocyte function observed in this patient.

B-Lymphocytes↗
PubMed1982

Induction of suppressor cells after activation of human peripheral blood mononuclear cells with sodium periodate.

Pretreatment of normal human peripheral blood mononuclear cells (MN) with sodium periodate (NaIO4) resulted in the induction of suppressor cells. The mitogenic response of fresh allogeneic and autologous cells to phytohaemagglutinin (PHA), Concanavalin A (Con A), pokeweed mitogen (PWM), various antigens and in mixed lymphocyte culture was suppressed when NaIO4 pretreated cells were present. PWM-induced plaque-forming-cell responses were also suppressed by NaIO4-pretreated cells. Treatment of cells with mitomycin C before the NaIO4 treatment abolished the suppressive activity. A ratio of 1 : combination that resulted in the strongest suppression. Supernatants from NaIO4-pretreated cell cultures were not inhibitory.

Antibody Formation↗
PubMed1981

Mechanism of suppression of lymphocyte proliferation by Concanavalin A-activated mononuclear cells.

In this study, the mechanism by which Concanavalin A (Con A) pre-treated lymphocytes suppress mitogen-induced proliferation of responder cells was investigated. Responder-cell proliferation could only be suppressed when these cells were co-cultured with the Con A pre-treated cells but not with their supernatants, nor in chambers where the suppressor cells were separated from the responder cells by a millipore filter. Suppression could not be mediated by heat-killed Con A-activated cells or lysates from these cells. Trypsinization of the Con A-induced suppressor cells resulted in loss of suppressor activity which could be restored if the cells were allowed to recover overnight. Trypsinization of the responder cells, however, before their co-culture with the Con A pre-treated cells did not affect suppression. Addition of cytochalasin B to the co-culture resulted in reduced suppression and cycloheximide treatment of the suppressor cells abolished their activity. The results indicate that for optimal suppression to occur, cell-to-cell contact is required and viable, intact Con A-inducible suppressor cells, actively synthesizing protein are essential. Furthermore, suppression may be mediated via a membrane receptor on the suppressor cell as manipulations of normal membrane function may abolish suppression.

Concanavalin A↗
PubMed1981

Production of a suppressor factor by adherent cells from Mycobacterium tuberculosis-infected guinea-pigs.

Adherent cells from the spleen of guinea-pigs infected with Mycobacterium tuberculosis (M. tuberculosis) spontaneously released a factor which suppressed the blastogenic response of normal guinea-pig and human peripheral blood lymphocytes to PHA activation. Suppressor factor production was evident within 3 hr of culture, continued for 2 days and diminished thereafter. This effect was not observed in supernatants derived from normal guinea-pig splenic adherent cells or from peripheral blood adherent cells of both normal or M. tuberculosis-infected guinea-pigs. Analysis of the spontaneously generated adherent cell supernatant indicated that it activated a subpopulation of lymphocytes to become suppressor cells. We conclude that adherent cells phagocytosing M. tuberculosis at the site of the lesion release a factor which activates suppressor cells, and that these cells may be important in the cellular unresponsiveness which develops in animals or man with advanced tuberculosis.

Animals↗