The Journal of Allergy and Clinical Immunology

Our medical research library holds 7 studies published in The Journal of Allergy and Clinical Immunology (1976–1983). Each entry links to the study's record on PubMed and, where there is one, to the publisher's page and a free full text. 6 have an abstract, the authors' own summary as PubMed records it: open "Abstract" to read it. For 1 study PubMed has no abstract for, we give the abstract printed in the article or, where there is none, a summary we wrote from it, each labeled as such.

About the journal

• Publisher: Mosby
• Published: 1971 to the present, United States
• Language: English
• ISSN: 0091-6749 (print), 1097-6825 (electronic)
• Continues: Journal of Allergy
• Its record in the NLM Catalog

1980s

• Analysis of depressed cell-mediated immunity in asbestos workers. R.D. deShazo, J. Nordberg, Y. Baser, et al. 1983;71(4):418-24. PubMed · Publisher

  Abstract

  To explore the mechanisms of asbestos-related perturbations of the immune system, we evaluated the in vitro cell-mediated immunity of five asymptomatic asbestos workers with hypergammaglobulinemia and decreased T-cell numbers. These results were compared with those in 10 matched controls. Analysis of T-lymphocyte populations revealed decreased absolute numbers of OKT4+ (helper/inducer) T cells in the peripheral blood and phytohemagglutinin (PHA)-stimulated mononuclear cell cultures of the workers. When chrysotile asbestos was added to PHA cultures, expansion of OKT4+ cell populations was disproportionately inhibited in workers' cultures. Furthermore, control proliferative responses to PHA became indistinguishable from initial worker responses. These effects were incompletely explained by the cytotoxic effects of asbestos on cultured lymphocytes. We conclude that both in vivo and in vitro exposure of mononuclear cell populations to asbestos may lead to a diminution of helper-inducer T-cell numbers. In asbestos-exposed individuals, this latter lymphocyte subpopulation appears to be especially sensitive to in vitro asbestos exposure. Although the clinical implications of these findings are unclear, we hypothesize that many of the immunologic abnormalities that occur in asbestos workers could be explained by direct asbestos effects on the OKT4+ immunoregulatory population.

• Humoral immunologic abnormalities in workers exposed to asbestos cement dust. N.J. Doll, J.E. Diem, R.N. Jones, et al. 1983;72(5 Pt 1):509-12. PubMed · Publisher

  Abstract

  Serum specimens from 144 workers exposed to asbestos cement dust were examined for the presence of ANA, RF, immunoglobulins, and IC. These immunologic findings were compared with chest radiographic changes. A high percentage of workers had polyclonal hypergammaglobulinemia, and there was a statistically significant association between elevated levels of IgG and IgM and radiographic classification. Although a significant number of workers had an increased prevalence of ANA and elevated levels of IC, there was no correlation between these parameters and chest radiographs. These findings support B cell hyperactivity in workers exposed to asbestos and suggest that autoantibody production and IC are not directly involved in disease pathogenesis.

• Immunologic aberrations in asbestos cement workers: dissociation from asbestosis. R.D. deShazo, D.J. Hendrick, J.E. Diem, et al. 1983;72(5 Pt 1):454-61. PubMed · Publisher

  Abstract

  Immunoregulatory disorders have been implicated in the pathogenesis of asbestosis. We therefore compared the immunologic status of a well-characterized group of 31 current and former asbestos-cement workers with that of a group of 52 healthy controls, after adjustments had been made for the possible confounding effects of age, race, and smoking. The asbestos workers had significantly decreased percentages and numbers of both B and T lymphocytes in peripheral blood and a paradoxical IgG hypergammaglobulinemia. Analysis of T-lymphocyte subpopulations revealed that total T-cell numbers (OKT3+), helper-inducer T-cell numbers (OKT4+), and suppressor-cytotoxic T cell numbers (OKT8+) were decreased by similar proportions. These decreases were negatively correlated with time elapsing since the end of exposure to asbestos. In both workers and controls, lymphocyte proliferative responses to phytohemagglutinin (PHA) were correlated positively with the number of OKT4+ cells and negatively with age and serum IgG levels. When adjustments had been made for these confounding variables, no differences in PHA responses were noted between workers and controls. No relationship was detected in the workers between any of the immunologic aberrations noted and (1) radiographic category of pneumoconiosis, (2) estimates of cumulative asbestos exposure, or (3) abnormalities of pulmonary function. These data suggest that the immunologic perturbations we have noted in asbestos-exposed individuals are epiphenomena, unrelated to the pathogenesis of asbestosis itself.

• Current concepts about the pathogenesis of silicosis and asbestosis. R.D. deShazo. 1982;70(1):41-9. Review PubMed · Publisher

  Abstract

  Silicosis and asbestosis are two forms of fibrotic lung disease resulting from the inhalation of inert materials indigestible by pulmonary alveolar macrophages. Results of studies of the host response to these particulates have not always been consistent. It is clear, however, that after phagocytosis, both cause alveolar macrophage damage, with resultant release of macrophage products, including fibrogenic factors and chemotactic factors for neutrophils. The latter cells also release lysosomal enzymes and free radicals when exposed to silica and asbestos. The net effect of these observations suggests that the combination of tissue damage and fibroblast stimulation results in the pulmonary fibrosis characterizing these diseases. Patients with silicosis and asbestosis have normal or decreased cell-mediated and increased humoral immunity with a high incidence of circulating immune complexes and autoantibodies. Whether these abnormalities are related to the pathogenesis of pulmonary fibrosis or are epiphenomena remains to be determined.

1970s

• Binding of immunoglobulin and activation of complement by asbestos fibers. P. Hasselbacher. 1979;64(4):294-8. PubMed · Publisher

  Abstract

  Asbestos fibers adsorbed IgG from whole human serum in amounts comparable to that taken up by crystals of calcium pyrophosphate or hydroxyapatite, but less than that adsorbed by crystals of monosodium urate monohydrate. Chrysotile asbestos was much more active in binding IgG than was amphibole asbestos. The electrophoretic mobility of adsorbed IgG was a function of the surface charge of the crystal studied. Negatively charged fibers adsorbed cationic IgG, and positively charged fibers adsorbed anionic IgG. Complement activation by asbestos, as judged by electrophoretic conversion of C3, was similar for all fiber types tested. Properdin factor B was also activated in the presence of asbestos. Activation of both properdin factor B and C3 was only partially inhibited by ethylene glycol tetraacetic acid, demonstrating that activation was occurring through both the classical and alternative pathways.

• Activation of the alternative complement pathway and generation of chemotactic factors by asbestos. M.R. Wilson, H.R. Gaumer, J.E. Salvaggio. 1977;60(4):218-22. PubMed · Publisher

  Abstract

  Five types of asbestos plus silica and glass wool fibers were tested for their ability to activate the alternative complement pathway and to generate chemotactic factor activity from fresh normal human serum (NHS). Two assays were used to detect alternative pathway activation by the fibers. The first method was a hemolytic assay that utilized glutathione-sensitized human erythrocytes (GSHE) to detect the C5b-C9 complexes generated by activation of fresh NHS with the various fibers. The second method was an immunoelectrophoretic assay to detect split products of activation of factor B after the fibers were incubated with NHS. Both assays were performed under conditions that have been shown to block the initial steps of classical pathway activation but permit activation of the alternative complement pathway. All five asbestos fibers tested, amosite, anthophyllite, crocidolite, and chrysotiles A and B activated the alternative pathway when tested by both methods. In addition, it was demonstrated that chemotactic factor activity was generated when asbestos fibers were incubated with fresh NHS. In contrast, silica and glass wool fibers did not activate the alternative complement pathway and did not generate chemotactic factor activity. These observations suggest that the complement system may mediate the initial inflammatory response observed upon exposure to certain types of asbestos fibers.

  PubMed has no abstract for this study. This is the authors' abstract, copied from the article.

• Possible asbestos hazards in clinical allergy. I.L. Bernstein, J. Moteff. 1976;57(5):489-92. PubMed · Publisher

  Abstract

  The potential hazards of biological products contaminated by asbestos fibers are quite properly being reviewed by the food and pharmaceutical industries. We have demonstrated that glycerinated saline solutions can be contaminated with asbestos fibers under certain conditions of simulated clinical use of asbestos-packed syringes. Because the fibrogenic and carcinogenic effects of asbestos are subtle and may not be manifest for a long latent period, the future use of asbestos containing materials in allergy practice might be more harmful than now realized.

Browse every journal in the library or the library by type of article, or return to medical research.