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Biomedical subjects

A R Rabson

Publications and source records attributed to A R Rabson.

At least 73 records · Page 4Linked to original sources
PubMed1981

Production of a suppressor factor by human adherent cells treated with Mycobacterium tuberculosis: absence in systemic lupus erythematosus.

When human peripheral blood mononuclear cells are activated by mitogens in the presence of Mycobacterium tuberculosis (M. tuberculosis), considerable suppression of 3H-thymidine incorporation is observed. Proliferation of mononuclear cells from patients with SLE was not suppressed by treatment with mycobacteria. Analysis of suppressor effect indicated that normal peripheral blood adherent cells treated with mycobacteria release a soluble factor which activates a precursor cell population to become active suppressor T cells. Although lymphocytes from patients with SLE were responsive to suppressor factor produced by normal adherent cells treated with mycobacteria, SLE adherent cells were incapable of producing suppressor factor when treated in the same way. In order to determine whether the inability of SLE adherent cells to produce suppressor factor was due to the presence of immune complexes on the surface of these cells, SLE adherent cells were trypsinized or preincubated prior to treatment with mycobacteria. Neither of these manoeuvres restored the ability of SLE adherent cells to produce suppressor factor. Furthermore, normal adherent cells continued to produce the factor after prior treatment with varying concentrations of human serum albumin-anti-human serum albumin complexes. The results suggest that a basic adherent cell defect exists in SLE and that under certain circumstances this may give rise to a secondary defect of suppressor cell activation.

Adolescent↗
PubMed1980

Hyperimmunoglobulinaemia associated with absent suppressor cells, aplastic anaemia and trisomy 8.

A child with aplastic anaemia and trisomy 8 in bone marrow cells was observed to have extremely high levels of circulating immunglobulins. Concanavalin A (con A)-inducible suppressor cells were assessed in the patient's peripheral blood by their ability to suppress both the proliferative response of normal allogeneic cells activated in a two-way mixed lymphocyte culture with and without added phytohaemagglutinin (PHA) and the ability of normal allogeneic cells to produce the lymphokine leucocyte inhibitory factor when activated by PHA. Con A consistently failed to induce suppressor cells from the patient but not from control lymphocytes. It is suggested that the lack of suppressor cells may account for uncontrolled B-cell proliferation and associated hypergammaglobulinaemia.

Anemia, Aplastic↗
PubMed1980

Production of a suppressor factor by human adherent cells treated with mycobacteria.

Human peripheral blood mononuclear cell (MN) proliferation and lymphokine production induced by mitogen could be inhibited by heat killed whole mycobacteria. The inhibition was induced by a wide variety of mycobacteri but not by other Gram-positive or Gram-negative organisms or by latex particles. Proliferation and lymphokine production by adherent cell-depleted lymphocytes was not inhibited by these organisms. Adherent cells treated with mycobacteria had the ability to inhibit lymphocyte blastogenesis when co-cultured with the lymphocytes. the inhibitory effect of these adherent cells was due to the release of a heat stable, nondialyzable suppressor cells. These latter cells, which were T gamma cells, could inhibit the blastogenic ability of normal lymphocytes activated by mitogens. The results suggest that in situations of high mycobacterial load, adherent cells are activted to release a suppressor factor that will activate lymphocytes to become suppressor cells. This mechanism may explain the anergy associated with lepromatous leprosy or advanced tuberculosis.

Cell Adhesion↗
PubMed1979

Desensitization of patients with bee sting allergy using pure bee venom.

Forty patients who had previously experienced severe systemic reactions after a bee sting were desensitized using pure bee venom. A modified 'Rush' regimen was employed whereby patients received two injections a week and reached maximal desensitization in 5 weeks. Eleven patients have subsequently been stung again and have developed no generalized reaction. Although this form of desensitization is considered to be highly effective in protecting sensitive patients, both generalized and local side-effects were frequent. Maintenance desensitizing injections are required every month for an indefinite period. It is concluded that desensitization with pure been venom should be undertaken only in highly selected sensitive patients, and should be performed under strict control.

Adolescent↗
PubMed1979

Evaluation of leucocyte adherence inhibition in hepatocellular carcinoma.

The value of the leucocyte adherence inhibition (LAI) test in the diagnosis of hepatocellular carcinoma (HCG) was investigated in 36 patients with this tumour. The sensitivity and specificity of the tube LAI test was assessed in 21 patients with HCC, 15 apparently healthy individuals, 9 patients with various forms of benign liver disease and 5 patients with non-hepatic neoplasms. In only 42% of the HCC patients tested was leucocyte adherence to glass reduced to a greater extent than in the healthy controls and in the patients with non-hepatic neoplasms, and the differences were not statistically significant. Moreover, positive results were obtained in 6/9 patients with benign hepatic disease. A further 15 patients were tested against extracts of HCC tissue using the haemacytometer LAI method. Of these, 53% gave positive results. In all, only 17/36 patients (47%) gave positive LAI responses. The test is thus of limited value in the diagnosis of HCC. The high false-negative result rate may be due either to abrogation of the immune response in HCC patients with large tumour burdens or to antigenic heterogeneity in HCC.

Adult↗
PubMed1979

Further evidence for independent segregation of the HLA system and a structural gene for the sixth component of complement (C6).

Previous studies have shown conflicting results with respect to the relationship between C6 deficiency and the HLA system. The present investigation of two kinships, in which C6 deficiency was associated with the expression of an amorphic (or silent) C6 allele, has provided further evidence for the genetic independence of a structural C6 locus and the HLA system.

Adult↗
PubMed1978

The effect of levamisole on E-rosette formation by trypsinized lymphocytes.

Normal lymphocytes treated with trypsin lost their ability to form normal numbers of rosettes with sheep red blood cells. The recovery in E-rosette forming capacity of trypsinized cells was considerably augmented when the cells were incubated in the presence of a wide range of concentrations of the immunostimulatory drug, levamisole. Substantial recovery of rosette-forming ability was seen 2 hr after incubation of trypsinized cells with levamisole.

Humans↗
PubMed1978

Inhibitory effect of prostaglandin A1 on neutrophil motility.

Using Boyden chambers, Prostaglandin A1 (PGA1) was shown to inhibit directed movement of polymorphonuclear (PMN) leucocytes to the chemoattractants endotoxin-activated serum and casein, and in random migration systems. Depressed chemotaxis could not be entirely attributed to defective random migration, as the drug was shown to inhibit both chemokinesis (stimulated random migration) and "true chemotaxis". In addition, PGA1 inhibited the movement of neutrophils out of capillary tubes and substantially reduced hexose monophosphate shunt (HMPS) activity. Mice injected with PGA1 demonstrated significantly less PMN movement into trypticase-soy-broth-induced peritoneal exudates, and it is postulated that during inflammatory processes release of PGA1 increases cell accumulation at the site, thereby amplifying the inflammatory response.

Chemotaxis, Leukocyte↗
PubMed1978

The effect of chemotactic factors and agents which influence neutrophil movement on anaerobic glycolysis and hexose monophosphate shunt activity.

The effects of two chemotactic factors, endotoxin activated serm (EAS) and casein and a number of drugs known to affect intracellular cyclic nucleotide levels and various froms of neutrophil movement, on neutrophil anaerobic glycolysis and hexose monophosphate shunt (HMPS) activity were assessed. EAS caused stimulation of glycolysis. HMPS activity and NBT reduction, but casein was without effect on glycolysis and NBT reduction and inhibited HMPS activity. Drug known to increase intracellular cAMP levels caused a depression of HMPS activity whereas those reported to elevate cGMP had a variety of effects. Glycolysis was not affected by any of these agents. These results indicate a lack of relationship between cyclic nucleotide effect on cell motility and neutrophil glycolysis and HMPS activity.

Caseins↗
PubMed1978

Defective neutrophil motility and recurrent infection. In vitro and in vivo effects of levamisole.

Eighteen patients with primary abnormalities of neutrophil chemotaxis are described. The most common clinical presentation was one of recurrent upper respiratory tract infection (nine patients) or recurrent pyoderma (seven patients), and two children had a history of oropharyngeal candidiasis and recurrent skin sepsis. Of these eighteen patients, sixteen had intrinsic polymorphonuclear leucocyte (PMN) defects as shown by diminished random migration and movement towards endotoxin-activated serum. PMN chemotaxis towards casein was, however, normal. In nine out of the latter patients, there was an associated inability of the serum to generate chemotactic factors. PMN from two adult patients, both suffering from recurrent boils, moved normally both in random and directed systems, but sera from these patients contained heat-stable inhibitors of neutrophil chemotaxis. In vitro levamisole treatment (10(-3) M) markedly improved the PMN function. When patients were treated with levamisole, however, no clinical response was noted, although PMN movement improved in a number of cases.

Adolescent↗
PubMed1977

Depressed neutrophil motility in patients with recurrent herpes simplex virus infections: in vitro restoration with levamisole.

The random migration and chemotaxis of neutrophils from 10 patients with recurrent infections with herpes simplex virus were assessed. Chemotaxis to endotoxin-activated serum was markedly diminished in this group, but random migration was only mildly reduced, and chemotaxis to hydrolyzed casein was normal. The effects of the immunostimulant drug levamisole on the chemotaxis of neutrophils were assessed both in vitro and in patients after 150 mg of the drug was taken daily for three days. The defective chemotactic response could be corrected in vitro by treatment of the neutrophils with 10(-3) M levamisole. Of 10 patients treated with levamisole, five showed improved chemotaxis after three days, but no improvement in neutrophil function was observed in the other patients.

Cell Movement↗