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Biomedical subjects

A Basten

Publications and source records attributed to A Basten.

At least 127 records · Page 7Linked to original sources
PubMed1983

Acquired immune deficiency syndrome. A prodromal form.

Only one case of the acquired immune deficiency syndrome (AIDS) has been conclusively documented in Australia despite a large at-risk population and the endemic nature of the syndrome in the United States. In this article, the cases of two homosexual men who had the clinical and laboratory features of a prodromal form of AIDS are presented. Such cases should serve to alert the medical profession and public health authorities to the possible existence of the syndrome in Australia.

Acquired Immunodeficiency Syndrome↗
PubMed1983

Suppressor T cell memory. II. The role of memory suppressor T cells in tolerance to human gamma globulin.

The transient presence of suppressor T cell (Ts) activity in high-dose tolerance to human gamma globulin (HGG), and its (apparent) absence in low-dose tolerance, have been advanced as strong evidence against the concept that Ts play an important role in maintenance of immunological unresponsiveness. To analyze this question, CBA mice were exposed to high or low doses of deaggregated HGG (dHGG) and later challenged with HGG in immunogenic form (aHGG); their capacity to mount a primary or secondary suppressive response was assessed in an adoptive hapten-carrier system. Primary suppression reached a maximum 7 d after high-dose tolerance induction and gradually waned thereafter, being no longer detectable by day 30-35. Subsequent challenge of tolerant mice with aHGG, however, led to a rapid reactivation of suppression that bore the hallmarks of an anamnestic secondary response, and this effect was still demonstrable 135 d after tolerance induction. It was also shown that a single low dose of dHGG was capable of generating memory for suppression despite the absence of detectable primary suppression, indicating that the latter is not a prerequisite for induction of memory cells. The results were interpreted as indicating that tolerance, like immunity, is a manifestation of specific immunological memory. If tolerance to self-antigens is maintained by a similar mechanism, it would be expected that memory Ts could be induced during the early stages of fetal development. Mice were therefore exposed to tolerogen in utero by injection of their mothers with dHGG at day 7 of gestation, and were assessed at various times after birth for the capacity to exhibit primary or secondary suppression in adoptive transfer. Nonspecific suppression masked any specific effects during the first 5 wk of life. Antigen-specific, primary suppression was demonstrable subsequently until 10-12 wk of age, and if the animals were challenged with aHGG before transfer an anamnestic secondary suppressive response could be elicited up to 6 mo of age. These observations are consistent with the notion that memory Ts may play an important role in the maintenance of self-tolerance.

Animals↗
PubMed1983

Standardization of antigen E in ragweed pollen extracts using a monoclonal antibody-based enzyme immunoassay.

A hybridoma-derived monoclonal IgG antibody specific for ragweed AgE was used to develop a competitive binding enzyme immunoassay suitable for quantitation of antigen E levels in ragweed pollen extracts. The assay was capable of detecting as little as 30 ng/ml AgE in crude pollen extracts. The monoclonal antibody was shown to react with AgE present in commercial pooled pollen extracts from a number of ragweed species as well as a laboratory extract from a single species. In contrast to previous conventional xenoantisera, it could distinguish true ragweed (Ambrosia sp) from false ragweed (Franseria sp). The use of monoclonal antibodies in assay systems such as this offers a reproducible and widely applicable method for allergen standardization.

Allergens↗
PubMed1982

Loss of secretion in mouse-human hybrids need not be due to the loss of a structural gene.

Three cloned mouse-human lines (B1-29, E2-42, and A2-31) secreting human immunoglobulin (Ig) were obtained from a fusion between the mouse myeloma line NS-1 and human tonsillar lymphocytes stimulated in vitro with pokeweed mitogen. One line, B1-29, has continued to secrete human IgG for a period of 2 yr in culture. This line was recloned three times to give a panel of secreting and nonsecreting subclones. Most of the nonsecreting subclones had also lost surface Ig. The structural genes for human Ig heavy chains have been provisionally assigned to chromosome 14, which also encodes the enzyme nucleoside phosphorylase. Human nucleoside phosphorylase was detected in all secreting and nonsecreting B1-29 subclones, indicating the presence of human chromosome 14. The retention of chromosome 14 in nonsecreting clones implied that the structural genes for human Ig were A2-31 and E2-42, which had stopped secreting, an attempt was made to restimulate the secreting of human Ig with mitogens A2-31 was unique among the cell lines examined, in that chromosome 14 could not be detected by an isoenzyme marker. Lipopolysaccharide, at an optimum dose of 10 micrograms/ml, restimulated these nonsecreting hybrid lines to secrete human IgG in levels up to 0.7 micrograms/ml. Loss of Ig secretion may not therefore be caused by loss of Ig structural genes.

Animals↗
PubMed1981

HLA family studies and multiple sclerosis: A common gene, dominantly expressed.

All available Australian families with more than one member suffering multiple sclerosis (MS) were HLA typed. As with all other individual published studies, convincing evidence for linkage between the HLA system and disease was not obtained. An analysis of 100 published affected sib-pairs and 17 cousin-pairs, however, established the existence of an HLA-linked disease susceptibility gene for MS, which is likely to be dominantly expressed. Dominance was also supported by the finding of only three HLA-DR2 (Dw2) homozygous individuals out of 60 unrelated patients which enabled rejection of a recessive gene hypothesis (p less than 0.02). Analysis of the sib-pair data strongly suggested that this MS gene is not rare in the normal population and may be as common as DR2.

Australia↗
PubMed1981

Investigation of the possible involvement of IgE anti-salicyloyl antibodies in patients with urticaria.

19 aspirin-sensitive and 14 non-aspirin-sensitive patients with chronic urticaria were tested for the presence of specific anti-salicyloyl-IgE antibodies by prick testing, RAST and in vitro histamine release using an aspirin-polylysine conjugate. Polylysine succinate served as a control. Negative results were obtained in all cases with the exception of 1 patient who gave a positive prick test response. However, this patient reacted to the control conjugate as well as aspirin polylysine. Skin prick test responses to the battery of environmental allergens revealed that the majority (90%) of the aspirin-sensitive patients were non-atopic. The findings suggest that the clinical symptoms and signs in patients with chronic urticaria associated with aspirin sensitivity are not mediated by specific IgE antibodies.

Aspirin↗
PubMed1981

Alterations in T gamma cells in patients with chronic idiopathic thrombocytopenic purpura.

The number and percentage of T cells bearing Fc gamma receptors (T gamma) was quantitated in peripheral blood of patients with the autoimmune disease chronic ITP. In over half the patients, low initial percentages were obtained, the great majority of which returned to within the normal range after incubation under capping conditions. The phenomenon could be reproduced by pretreating normal T cells with immune complex containing sera or aggregated HGG. Furthermore, a reversible reduction in T gamma cells was observed in control patients with nonimmune thrombocytopenia and in pregnancy. In each case an association was observed between the reduced T gamma cell levels and the presence of circulating immune complexes, which suggested that the results could be explained by masking of Fc gamma receptors with preformed IgG-containing complexes. By contrast, patients with other autoimmune diseases such as scleroderma and rheumatoid arthritis had high or normal numbers of T gamma cells, respectively. Taken together, the findings do not support the existence of a gross deficiency of suppressor cells in patients with autoimmune disease and emphasize the need for caution in selection of markers for identification of T cell subsets.

Animals↗
PubMed1981

Disordered immune homeostasis in chronic idiopathic thrombocytopenic purpura.

A T:B co-culture system was used to test for the presence of disordered immune homeostasis in the autoimmune disease, chronic idiopathic thrombocytopenic purpura (ITP). Various numbers of T cells were added to a fixed number of B cells in the presence or absence of the polyclonal activator, pokeweed mitogen, and IgG production measured in the culture supernatants 6 days later. The results demonstrated a defect in T cell-dependent suppression and/or a state of B cell hyper-responsiveness in lymphocytes from patients compared to normal controls. The loss of T cell-dependent suppression could not be readily explained in terms of the therapy being used nor by the presence of circulating IgG containing immune complexes. The findings of a similar abnormality in some cases of non-immune thrombocytopenia suggested that the reduction in suppression observed in chronic ITP was unlikely to be a primary event in disease pathogenesis, although it could well contribute to the ongoing autoimmune response.

Adult↗
PubMed1980

Transfer factor in treatment of multiple sclerosis.

A 2-year prospective double-blind trial of the treatment of multiple sclerosis patients with the leucocyte extract, transfer factor (TF), obtained from leucocytes of relatives living with the patient, was conducted. 60 patients with definite MS, of whom 58 completed the trial, were divided into two equal groups, one of which received TF and the other placebo. The groups were evenly balanced with respect to sex ratios, disability, duration of disease, ratio of moderate to severe cases, and HLA phenotype. Neurological, electrophysiological, and immunological assessments were done at the start of the trial and every 6 months thereafter. The results indicated that (1) TF retarded but did not reverse progression of the disease; (2) a significant difference between treatment and placebo groups was not apparent with 18 months after the start of the trial; and (3) treatment was effective only in those patients with mild to moderate disease activity.

Adolescent↗