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Biomedical subjects

A R Rabson

Publications and source records attributed to A R Rabson.

At least 37 records · Page 2Linked to original sources
PubMed1987

A double-blind study comparing monomethoxy polyethylene glycol-modified honeybee venom and unmodified honeybee venom for immunotherapy. I. Clinical results.

Thirty-five patients were allocated at random to immunotherapy (IT) in a double-blind way with either monomethoxy polyethylene glycol (mPEG)-modified honeybee venom (HBV) or HBV. The two groups were well matched regarding age, sex, skin sensitivity, HBV-specific serum IgE and IgG antibodies, and history of reactions after a field sting; mPEG-HBV-treated patients received doses that increased more steeply than doses of the HBV-treated patients. The maintenance dose of the former group (200 micrograms) was greater than that of the latter group (100 micrograms). During IT, both groups had the same frequency of local swellings after injections. Four patients receiving mPEG-HBV developed one mild systemic reaction (SR) during dose increase, whereas 10 patients receiving HBV demonstrated one or more of these reactions, compelling two patients to stop therapy. Following challenge with a honeybee sting after about 14 weeks of IT, six patients with SR were observed, four in the mPEG-HBV-treated group and two in the HBV-treated group. In the HBV-treated group, three patients were not challenged, one because of an insufficient IgG increase and two other patients because they dropped out of IT before reaching maintenance dose because of repeated SRs. Since the mPEG-HBV is extremely well tolerated during IT and the success rate is not significantly lower than with unmodified HBV, we suggest it as an attractive alternative to HBV for the treatment of HBV hypersensitivity. Increase of the maintenance dose may result in an even better clinical efficacy.

Adolescent↗
PubMed1987

The late onset form of C1 esterase-inhibitor deficiency presenting as food allergy.

Two cases of late onset recurrent angioedema associated with deficiency of C1 esterase inhibitor are described. Both patients had life-threatening episodes of angioedema that they had related to the ingestion of certain foodstuffs. This was not confirmed by food challenges or by food allergy skin testing, although both patients had embarked on strict exclusion diets before the diagnosis of C1 esterase-inhibitor deficiency. Clinicians should be aware of the entity of late onset angioedema caused by C1 esterase deficiency mimicking food allergy and hence delaying the diagnosis of this potentially lethal condition.

Aged↗
PubMed1987

Development of specific IgE antibodies after repeated exposure to snake venom.

A patient who had been working with snakes for many years developed urticarial lesions on contact with the venom of the poisonous rinkals (Haemachates haemachatus). More recently, the patient complained of generalized allergic reactions occurring within minutes of exposure to the venom. The patient's serum, but not control sera, contained IgE antibodies that reacted with the specific snake venom in an ELISA and was demonstrated to associate with a 66 kd component of the venom with Western blotting. With an ELISA, the patient's serum was also demonstrated to contain IgG antibodies to the specific snake venom and to venom from three other snakes with which the patient had previously been in contact. The possibility of an acute allergic reaction should be considered in individuals continuously working with snakes or in individuals who have previously been bitten by snakes.

Adult↗
PubMed1987

Gamma interferon reverses inhibition of leukocyte bactericidal activity by a 25-kilodalton fraction from Mycobacterium tuberculosis.

In this study we examined the effects of Mycobacterium tuberculosis cell extracts on the phagocytic activity of polymorphonuclear leukocytes and cultured peripheral blood monocytes. M. tuberculosis cell extracts were fractionated on Sephacryl S-200 columns, and a 25-kilodalton glycolipoprotein was shown to inhibit the intracellular killing ability of these leukocytes but had no effect on their phagocytic potential. This same fraction inhibited fusion of phagosomes with lysosomes, as assessed by noting the transfer of acridine orange from lysosomes to phagosomes. This fraction was shown to have a maximal inhibitory effect when it was in the form of an intact carbohydrate-lipid-protein complex. Gamma interferon (IFN-gamma), but not IFN-alpha, reversed the inhibitory effect of the mycobacterial component on bactericidal activity and on fusion of phagosomes and lysosomes. Thus, this 25-kilodalton fraction of M. tuberculosis cell extract may be important in protecting organisms against phagocytic degradation, an effect which can be reversed by IFN-gamma.

Bacterial Proteins↗
PubMed1987

Depressed 3H-thymidine incorporation by measles infected mononuclear cells can be corrected by treatment with isoprinosine or 5-fluoro-2-deoxyuridine.

Incorporation of thymidine by measles infected PHA-activated lymphocytes was found to be depressed although production of interleukin 2 (IL-2) and expression of IL-2 receptors on these cells was similar to that of non-infected cells. The decrease in incorporation of 3H-thymidine by infected cells was not due to cell death and could be restored by treating the cells with isoprinosine or 5-fluoro-2-deoxyuridine. These results suggest that the depressed incorporation of 3H-thymidine by measles-infected cells is not due to inhibition of early events required for lymphocyte proliferation, but is rather due to interference in the thymidine pathway required for the synthesis of DNA.

Antigens, Surface↗
PubMed1986

The effect of RU 41.740 (Biostim) on the production of interleukin-1 by monocytes and enriched large granular lymphocytes in normals and patients with hepatocellular carcinoma.

The effect of RU 41.740 on natural killer (NK) cell cytotoxicity from normals and patients with advanced hepatocellular carcinoma (HCC) was studied. RU 41.740-treated normal enriched large granular lymphocytes (LGLs) showed increased cytotoxic activity against 51Cr-labelled K562 cells. Although the drug increased the cytotoxic activity of LGLs from HCC patients, these results were not statistically significant. As LGLs have been shown to release interleukin-1 (IL-1) after suitable stimulation the effects of RU 41.740 on production of this cytokine from both monocytes and LGLs was studied. The drug stimulated IL-1 release from normal cells but monocyte and LGL IL-1 production from HCC patients was not influenced by RU 41.740 by RU 41.740. It is concluded, therefore, that although RU 41.740 can stimulate natural cytotoxicity and IL-1 production by normal LGLs, it is unable to correct the defect which exists in these functions in patients with large mass tumours.

Adjuvants, Immunologic↗
PubMed1986

Tumor cells stimulate interleukin 1 (IL-1) production from enriched large granular lymphocytes.

When enriched large granular lymphocytes (LGLs) were activated by K562 cells substantial amounts of interleukin 1 (IL-1) could be detected in the supernatants as measured by the mouse thymocyte assay. IL-1 could also be produced by LGLs treated with other tumor cells according to their ability to be lysed by LGLs. Therefore PLC/PRF/5 hepatoma cells which were moderately sensitive to LGL attack stimulated moderate amounts of IL-1 from the LGLs. Yac-1 cells and human fibroblasts which are resistant to LGL cytolysis did not activate LGLs to produce significant amounts of IL-1. IL-1 was shown to be produced by LGLs and not by the stimulatory tumor cells. Interferon-alpha (IFN), which reduced the susceptibility of target cells to be lysed by LGLs, also inhibited their ability to stimulate IL-1 production from LGLs. The IL-1 stimulatory effect of tumor cells on LGLs could not be attributed to Mycoplasma or endotoxin contamination. It is suggested that LGLs release IL-1 when they encounter susceptible cells and that release of this cytokine is important in the subsequent lysis of target cells.

Animals↗
PubMed1986

Lack of responsiveness of beekeeper mononuclear cells to in vitro stimulation with pure bee venom.

Lymphocyte proliferation activity after in vitro bee venom (BV) stimulation was examined in a group of patients allergic to bee stings and in a group of beekeepers. Although the allergic patients responded strongly to increasing doses of BV, the beekeepers demonstrated no proliferative activity and an inability to produce interleukin-2 after BV stimulation. Removal of adherent cells or various populations of suppressor cells, including T gamma cells and OKT8 positive cells, did not influence the cellular unresponsiveness of cells of beekeepers after BV stimulation. Furthermore, cells of beekeepers, when they were trypsinized or when they were preincubated for 72 hours, did not proliferate after BV challenge. It is concluded that the lack of proliferation of lymphocytes of beekeepers and the inability to produce interleukin-2 is not due to a suppressor mechanism or to the presence of anti-idiotype antibodies coating the surface of lymphocytes of beekeepers. The mechanism behind the failure of cells of beekeepers to proliferate remains unclear.

Adult↗
PubMed1986

Aberrant expression of HLA-DR antigen on valvular fibroblasts from patients with active rheumatic carditis.

Immunofluorescence and immunoperoxidase staining was used to investigate the expression of Class II major histocompatibility antigens in myocardial tissue of 16 patients with acute rheumatic carditis. Aberrant expression of HLA-DR was examined using monoclonal anti-Ia antibodies and was detected on the valvular fibroblasts of those valves with ongoing active carditis. Sections of myocardial and valvular tissue from normal controls or from patients dying of other cardiac diseases did not express HLA-DR. The aberrant expression of HLA-DR on valvular fibroblasts could be important in triggering autoimmune destruction in that these cells could present self-antigens to sensitized T-lymphocytes which could initiate autoantibody production or direct destruction of local tissue.

Acute Disease↗
PubMed1985

Desensitization of patients with bee venom allergy--current status.

Bee venom allergy is a common problem in South Africa, and although most patients develop only local reactions after a sting, generalized life-threatening reactions may occur. Immunotherapy with purified bee venom has proved effective in preventing subsequent sting anaphylaxis. However, because of side-effects during a course of desensitization, the high cost of this form of therapy and the extended period for which therapy may be required, careful patient selection is essential. Only patients with documented generalized reactions should be considered for therapy. Patients with severe local reactions, and those with urticaria or other cutaneous symptoms, should not undergo desensitization. Although it is not yet known for how long desensitization should continue, a negative skin test 3-6 years after the initiation of therapy suggests that desensitization can be discontinued.

Anaphylaxis↗
PubMed1985

Defective interleukin-1 production by natural killer cells of patients with cancer.

Large granular lymphocytes (LGLs) from patients with malignant disease and from controls were activated by endotoxin or K562 cells, and the supernatants assayed for interleukin-1 (IL-1) activity. Normal LGLs produced significant amounts of IL-1, the activity of which could be neutralized by anti-human IL-1 antiserum. In patients with advanced cancer depressed IL-1 production was observed, which generally correlated with the degree of cytotoxicity produced by the LGLs. Prior treatment of the LGLs with interferon increased production of IL-1 by both control and patient cells. It is suggested that LGLs coming into contact with K562 cells produce IL-1, which is important in the effector-target cell interaction. The decreased cytotoxic activity of LGLs from cancer patients could be related to a defect in IL-1 production, an effect which can be partially corrected by in vitro interferon treatment.

Adult↗
PubMed1985

Defective monocyte function in patients with systemic lupus erythematosus.

Peripheral blood adherent cells from patients with systemic lupus erythematosus (SLE) were shown to have markedly reduced phagocytic activity as compared to normal adherent cells or those from non-SLE patients receiving corticosteroid therapy. Both resting and phagocytosing monocytes showed decreased hexose monophosphate shunt and glycolytic activity. Mononuclear cells from SLE patients showed grossly impaired proliferative activity after NaIO4 activation. Furthermore, addition of SLE adherent cells to normal adherent cell-depleted lymphocytes decreased [3H]thymidine incorporation of the latter cells following NaIO4 treatment. Addition of normal adherent cells to SLE lymphocytes corrected the previous defect, indicating that an adherent abnormality is responsible for the defect in SLE mononuclear cell proliferation to NaIO4 activation.

Blood Bactericidal Activity↗
PubMed1985

Modulation of the sodium periodate (NaIO4) response in systemic lupus erythematosus (SLE): effect of interleukin-1 (IL-1), interleukin-2 (IL-2), phorbol myristate acetate (PMA), and indomethacin.

The proliferative activity of peripheral blood mononuclear cells (PBMN) from patients with systemic lupus erythematosus (SLE) activated by sodium periodate (NaIO4) is greatly diminished. The effect of the cytokines Interleukin-1 (IL-1) and Interleukin-2 (IL-2) on the NaIO4 reaction was investigated. Addition of IL-1 resulted in partial restoration of the reaction of SLE PBMN to NaIO4, and a similar effect was demonstrated in the presence of phorbol myristate acetate (PMA). Addition of IL-2 to NaIO4 activated SLE PBMN, however, caused a marked improvement in their proliferative activity. The presence of indomethacin resulted in only a slight increase in [3H]thymidine incorporation by the NaIO4-treated SLE cells. The results suggest that the defect in the response of SLE PBMN cells to NaIO4 is due to inadequate availability of IL-1 and IL-2. Excessive production of prostaglandin in SLE might also contribute to the defective response to NaIO4 but does not appear to play a major role.

Female↗
PubMed1985

The role of interleukin 1 (IL 1) in tumor-NK cell interactions: correction of defective NK cell activity in cancer patients by treating target cells with IL 1.

This study examined the importance of interleukin 1 (IL 1) in the large granular lymphocyte (LGL)-target cell interaction. K562 target cells when treated with highly purified human IL 1 for 1 hr bound greater numbers of LGL than untreated cells. LGL from patients with hepatocellular carcinoma (HCC) that bound few untreated K562 cells, attached to considerably increased numbers of IL 1-treated target cells. Cytotoxicity of LGL against target cells could similarly be increased by pulsing the latter cells with IL 1, and defective cytotoxicity of LGL from HCC patients could be corrected by treating the target K562 cells with IL 1. Lysis of PLC/PRF/5 cells, Yac-1 cells, and normal skin fibroblasts could also be increased by treatment with IL 1 for 1 hr. The enhanced binding and cytotoxicity of IL 1-treated target cells was only observed when the latter cells were preincubated with IL 1 at 37 degrees C, and was not evident at 4 degrees C. Furthermore, the IL 1-mediated effect could be abolished by treating the target cells with cycloheximide before the IL 1 pulse, or by adding rabbit anti-human IL 1 together with the IL 1. These results indicate that IL 1 affects a variety of target cells and increases their ability to bind and be lysed by enriched LGL. They demonstrate, furthermore, that defective natural cytotoxicity by the LGL of patients with advanced malignant disease can be corrected in vitro by treating the target cells with IL 1.

Adult↗
PubMed1984

Absence of OKT4-positive lymphocytes in black African subjects.

Some black Africans whose lymphocytes lack the OKT4 surface antigen, but which react with other monoclonal antibodies recognizing the human inducer T-cell subset are described. In addition, three members of a family showed lymphocytes which reacted weakly with the OKT4 antibody but reacted normally with the other monoclonal antibodies. Mitogen-induced proliferation of these cells as well as their ability to assist B lymphocytes to mature into antibody-producing cells was normal. Although the mode of inheritance of these variants of the OKT4 epitope cannot yet be determined, it appears as though these polymorphisms are not uncommon in black Africans.

Antibodies, Monoclonal↗
PubMed1984

Defective interleukin-1 production by monocytes from patients with malignant disease. Interferon increases IL-1 production.

Interleukin-1 (IL-1) production by monocytes of patients with various forms of malignant disease was measured after activating the cells with either lipopolysaccharide or malignant K562 cells. Monocytes from all the patients with large tumour masses, including 10 patients with hepatocellular carcinoma, produced considerably less IL-1 than controls or patients with small tumour burdens. After treating control or patient monocytes with human leucocyte interferon for 1 h prior to activation, IL-1 production was markedly improved. Depressed IL-1 production is, therefore, a further aberration in mononuclear function observed in patients with cancer.

Adult↗
PubMed1984

Suppression of interleukin-2 production by human concanavalin A-induced suppressor cells.

When PHA-activated normal responder cells (R cells) were cocultured with mononuclear cells (MN cells) which had been preincubated for 48 hr in medium alone (C cells) an enhanced proliferative response was observed. This enhancement was only obtained when the R cells were cultured with allogeneic C cells or when PHA was in the cocultures for the entire culture period. This effect was due to greater production of interleukin 2 (IL-2) by irradiated C cells in the presence of allogeneic or mitogenic stimulation. Con A-treated mononuclear cells (S cells) cultured with PHA-activated allogeneic or autologous responder cells showed reduced [3H]thymidine incorporation and IL-2 production as compared to activated R cells alone. Glutaraldehyde-treated S cells (which retained the ability to absorb IL-2) did not affect the proliferative response or IL-2 production by the R cells, indicating that passive absorption of IL-2 was not entirely responsible for suppression induced by S cells. S cells, pretreated with IL-2, still inhibited R-cell activity. These results show that Con A-treated MN cells suppressed or prevented [3H]thymidine incorporation by actively inhibiting IL-2 production.

Cell Communication↗