Clinical and Experimental Immunology

Our medical research library holds 21 studies published in Clinical and Experimental Immunology (1977–1994). 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. 20 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: Oxford University Press
• Published: 1966 to the present, England
• Language: English
• ISSN: 0009-9104 (print), 1365-2249 (electronic)
• Its record in the NLM Catalog

1990s

• Bacillus Calmette-Guérin (BCG) and immunoglobulins synergistically enhance mineral dust-induced production of reactive oxygen metabolites by human monocytes. P. Nyberg, M. Klockars. 1994;97(2):334-7. PubMed · Publisher · Free full text

  Abstract

  The modulating effect of BCG and polyclonal immunoglobulin on mineral dust-induced production of reactive oxygen metabolites (ROM) by human monocytes was studied using luminol-dependent chemiluminescence. BCG and immunoglobulin synergistically amplified the ROM production induced by chrysotile asbestos and quartz particles, and BCG caused a sharper dose response for poly-immunoglobulin added to the mineral dusts. Immunoglobulins did not affect zymosan yeast-induced ROM production, which was enhanced strongly by BCG. As there is evidence that phagocyte-derived ROM are of importance in mineral dust-induced lung injury, we suggest that the observed synergism between host response inflammatory mediators (poly-immunoglobulin) and exogenic irritants (BCG) may contribute to the outcome of exposure of mineral dusts, and thus in part explain the individual variations in susceptibility to mineral dust-induced diseases.

• Transforming growth factor-beta 1 (TGF-beta 1)- and beta 2-like activities in malignant pleural effusions caused by malignant mesothelioma or primary lung cancer. J. Maeda, N. Ueki, T. Ohkawa, et al. 1994;98(2):319-22. PubMed · Publisher · Free full text

  Abstract

  We investigated the levels of TGF-beta in malignant pleural effusions (MPE) caused by malignant mesothelioma (MESO) or primary lung cancer. TGF-beta levels in MPE caused by MESO were 283.9 +/- 219.2 pm (mean +/- s.d.) and were three to six times higher than those due to primary lung cancers (P < 0.01 or P < 0.05). We also evaluated TGF-beta 1- and beta 2-like activities in MPE using specific polyclonal antibodies. Although TGF-beta 1-like activity could be detected in all cases, TGF-beta 2-like activities were detected in five of seven in MESO and in a few cases with primary lung cancer. These results demonstrate that the levels of total TGF-beta and TGF-beta 2-like activity may be clinically useful to differentiate MESO from primary lung cancer. Our data also suggest that TGF-beta may help further characterize the clinical features of MESO.

• Tumour necrosis factor enhances the asbestos-induced production of reactive oxygen metabolites by human polymorphonuclear leucocytes (PMN). M. Klockars, H. Savolainen. 1992;90(1):68-71. PubMed · Publisher · Free full text

  Abstract

  We studied the effect of recombinant tumour necrosis factor-alpha (TNF-alpha) on the production of reactive oxygen metabolites (ROM) by human PMN exposed in vitro to chrysotile and crocidolite asbestos fibres, quartz dusts and opsonized zymosan. TNF caused a significant increase in ROM release by PMN, and significantly and dose-dependently amplified the ROM production induced by asbestos fibres. The amplification of ROM production by TNF can be of crucial importance in the process of lung inflammation and fibrogenesis in pneumoconioses.

• Asbestos fibres inhibit the in vitro activity of lymphokine-activated killer (LAK) cells from healthy individuals and patients with malignant mesothelioma. L.S. Manning, M.R. Davis, B.W. Robinson. 1991;83(1):85-91. PubMed · Publisher · Free full text

  Abstract

  Asbestos exposure is associated with an increased incidence of several malignancies, including malignant mesothelioma (MM). This study evaluates the relationship between asbestos exposure and the in vitro generation and function of LAK cells, an immune effector cell population with powerful lytic activity against MM cells. Both serpentine (chrysotile) and amphibole (amosite and crocidolite) forms of asbestos fibres suppress LAK cell generation, viability (by 5-11%, P less than 0.02) and cell recovery (by 13-15%, P less than 0.02). However, the LAK cells generated in the presence of the amphiboles were as effective as unexposed cells in lysing both standard tumour cell targets (K562, 56.4% lysis versus 61.5%, respectively, P greater than 0.5; NS; Daudi, 60.5% lysis versus 64.5% P greater than 0.5; NS), and MM tumour cell targets (mean of three MM cell lines 48.3% versus 46.3%, P greater than 0.5; NS), whereas the function of LAK cells generated in the presence of chrysotile was significantly reduced against three out of the five tumour cell targets tested (P less than 0.03). In the presence of asbestos fibres, LAK cell function was reduced against all five tumour cell targets (P less than 0.01), irrespective of whether the cell donors were healthy individuals or patients with MM. NK cell activity was also suppressed (P less than 0.01). The serpentine form of asbestos, chrysotile, was significantly more suppressive of both effector cell functions than either of the amphiboles (P less than 0.01). These findings suggest that asbestos exposure may suppress the function and in some instances the generation of immune effector cell mechanisms, thereby increasing the risk of disease and malignancy.

• Elevated binding activity of CD8+ cells with phytohaemagglutinin by asbestos fibre in vitro. K. Kinugawa, F. Hyodoh, A. Andoh, et al. 1990;80(1):89-93. PubMed · Publisher · Free full text

  Abstract

  Asbestos fibres are known to depress the mitogenic stimuli of phytohaemagglutinin (PHA) to lymphocytes. We examined effects of asbestos (chrysotile) fibre on the proliferation of PHA-stimulated lymphocytes and the PHA binding activity of lymphocytes in vitro. The incorporation of 3H-thymidine and the expression of interleukin-2 receptor were depressed when the cells were exposed to 50 micrograms/ml of chrysotile fibre. The PHA binding activity of lymphocytes was significantly enhanced after chrysotile fibre exposure, as compared with non-exposed group. These results indicate that the depression of PHA stimuli with chrysotile fibre was not due to blocking of PHA binding to lymphocytes. The enhancement of PHA binding activity by chrysotile fibre was observed on CD8+ but not on CD4+ cells. It is possible, therefore, that treatment of peripheral blood mononuclear cells with chrysotile fibre induces increased reactivity of CD8+ cells with PHA, and that intensely activated CD8+ cells suppress proliferation of lymphocytes.

1980s

• IgG and IgA enhance the chrysotile-induced production of reactive oxygen metabolites by human polymorphonuclear leucocytes. M. Klockars, M. Hedenborg, J. Koistinen, et al. 1989;78(3):372-7. PubMed · Free full text

  Abstract

  Chrysotile asbestos fibres induce a rapid generation of reactive oxygen metabolites by human polymorphonuclear leucocytes (PMNL) in vitro. This effect was markedly enhanced by the presence of 10-200 micrograms/ml of human gammaglobulin, purified polyclonal IgG, and monoclonal IgG and IgA myeloma proteins. Purified monoclonal IgD, IgM, kappa light chain proteins, and secretory IgA inhibited this chrysotile-induced response. No enhancing effect of IgG was observed when quartz dust or opsonized zymosan were used as stimulators of PMNL metabolism. The enhancing effect of IgG was shown to depend on opsonization of the asbestos fibre. We suggest that the IgG and IgA potentiating effect on the asbestos fibre-induced production of tissue-damaging reactive oxygen metabolites by inflammatory cells is dependent on a particle-specific binding of immunoglobulin to the fibre surface, with subsequent Fc receptor-mediated effects on cells. Such an interaction between certain immunoglobulins and asbestos may explain a number of in vivo phenomena in which immunological responses (hypergammaglobulinemia, circulating immune complexes, etc.) have been shown to relate to the progression of pulmonary asbestosis. The differences between various immunoglobulin classes and monoclonal immunoglobulins could represent an individual inflammation-modulating mechanism in the development of acute or chronic pulmonary asbestosis.

• Immunoregulation of lung fibroblast growth: alteration in asbestos-induced pulmonary fibrosis. I. Lemaire, C. Dubois, C. Grondin, et al. 1986;66(1):201-8. PubMed · Free full text

  Abstract

  Initial studies on mononuclear cell-fibroblast interactions have shown that stimulated human lymphocytes produced a fibroblast growth inhibitory factor and that asbestos, a fibrogenic dust, interferes with this process in vitro. To investigate the role of these interactions in pathologies characterized by pulmonary fibrosis, we used a rat model of asbestos-induced fibrosis. Rats received a single intratracheal instillation of either saline or 10 mg of chrysotile asbestos fibres. Three months after treatment, peripheral blood mononuclear leucocytes (PBML) supernatant fractions were prepared and their effects on lung fibroblast growth measured. As for human PBML, rat PBML stimulated with Concanavalin A (Con A) produced 24 h after initiation of the cultures a soluble factor which inhibits lung fibroblast DNA synthesis and growth in a dose-dependent fashion. By contrast, Con A-stimulated PBML from rats exposed to asbestos failed to produce significant levels of fibroblast growth inhibitory activity. No significant change of total PBML number or in the proportion of circulating mononuclear cell populations was observed. Furthermore, upon stimulation with lipopolysaccharide (LPS), monocytes from asbestotic animals retained their capacity to produce interleukin (IL-1), a mediator required for lymphokine production. Our study demonstrates that suppression of FGIF production by circulating PBML occurs in animals with lung fibrosis and suggests that mechanisms other than impairment of IL-1 production may be responsible for the suppressive effect of asbestos on the production of such fibroblast regulatory lymphokine.

• Immunotoxicology. K. Miller. 1985;61(2):219-23. Review PubMed · Free full text

  Summary

  This review, written at the British Industrial Biological Research Association, surveyed immunotoxicology, drawing on workshops and international meetings held between 1980 and 1984, including a 1984 International Seminar in Luxembourg. The author described the field as the study of adverse immune effects of xenobiotics and immunotherapeutic agents, allergenicity and autoimmunity caused by such exposures, and the use of immunological techniques in toxicology. The review discussed whether immune suppression by chemicals, many of them carcinogens, might contribute to cancer. Human examples included benzidine manufacturing workers, Michigan residents exposed to polybrominated biphenyls, and TCDD. Asbestos-associated disease was presented as a special case. Animal studies showed that asbestos effects on alveolar macrophages could produce sensitized T lymphocytes. Most clinical studies suggested impaired T lymphocyte function in people with asbestosis or pleural plaques. Studies of mesothelioma patients gave somewhat conflicting results but generally showed moderate to severe immune suppression. The author noted that studies of exposed human populations would have to be very large and long, and cited increased cancers in immunosuppressed patients. Other topics were drug-induced autoimmunity, biological response modifiers and monoclonal antibodies, and testing for contact hypersensitivity. The review also described two approaches to animal immunotoxicity testing: lymphoreticular histopathology in rats, used by the Dutch National Institute of Health, and functional and host-resistance assays in mice, under the US National Toxicology Program. The author concluded that the ideal assessment was still evolving. The review reported the Luxembourg Seminar's recommendation that validating and developing immunotoxicological methods be given priority, and called for cooperation between scientific institutions and industry.

  PubMed has no abstract for this study, and the article doesn't print one. We wrote this summary from the full article with the help of AI. It is not the authors' wording.

• Enhanced interleukin activity following asbestos inhalation. D.P. Hartmann, M.M. Georgian, Y. Oghiso, et al. 1984;55(3):643-50. PubMed · Free full text

  Abstract

  Asbestos inhalation can cause pulmonary fibrosis and is associated with a variety of immunological abnormalities. The purpose of this study was to evaluate the effects of asbestos inhalation on interleukin-1 (IL-1) and interleukin-2 (IL-2) production in a rodent model. Two groups of rats were exposed, by intermittent inhalation, to either amphibole (crocidolite) or serpentine (chrysotile) asbestos. A third (control) group of rats was sham exposed to clean air. Animals from the three exposure groups were thereafter immunized (or not immunized) with fetal calf serum antigens. In order to assay interleukin activity, supernatants were generated from cultures containing alveolar macrophages and autologous splenic lymphocytes, and from cultures containing alveolar macrophages alone. Using assay systems designed to detect IL-1 and IL-2 functional activity, the supernatants were evaluated for their capacity to stimulate lymphoproliferation and fibroblast DNA synthesis. Macrophage-lymphocyte co-culture supernatants, when obtained from immunized, asbestos exposed rats, contained greater IL-1 and IL-2 activity than identical supernatants from immunized, sham exposed animals. These between group differences were not, however, observed in supernatants from unimmunized rats, or when supernatants were generated in the absence of immune lymphocytes. These observations suggest that asbestos exposure is associated with enhanced activation of lymphocytes by antigens. The possible relevance of these findings to asbestos related fibrogenesis and immunological stimulation is discussed.

• Proliferation stimulating effects of chrysotile and crocidolite asbestos fibres on B lymphocyte cell lines. A. Ueki, T. Oka, Y. Mochizuki. 1984;56(2):425-30. PubMed · Free full text

  Abstract

  Asbestos fibres of chrysotile, crocidolite and amosite were incubated with eight types of human cell lines in vitro. These asbestos fibre were cytotoxic to fibroblasts and monocyte like cells, as is already known. On the other hand, immature B lymphocyte lines (B1 2) were stimulated significantly by chrysotile and crocidolite, while a mature B cell line (B3) was not affected. Cell proliferation of a T cell line and an erythromyeloid cell line also was not affected by asbestos. For the stimulation of lymphocytes, the binding of the mitogen to the reactive sites on the lymphocyte surface is thought to be indispensable. It seems that chrysotile and crocidolite asbestos can bind to immature B lymphocytes, but not to mature B cells.

• Pulmonary and systemic immunoregulatory changes during the development of experimental asbestosis. M. Rola-Pleszczynski, S. Gouin, R. Bégin. 1984;58(2):325-34. PubMed · Free full text

  Abstract

  Initial studies on the effects of low dose exposure to asbestos on pulmonary and systemic immune responses have revealed a bi-phasic pattern characterized by an early enhancement followed by inhibition of lymphocyte responses to several mitogens. In the present study, we sought to define the cellular and humoral factors, responsible for the observed effects. The early enhancement of peripheral blood and pulmonary lymphocyte responses to mitogens may be due, at least in part, to the loss of the inhibitory capacity of alveolar macrophages from asbestos exposed animals to suppress lymphocyte response. Furthermore, macrophages from low dose exposed animals actually enhanced lymphocytes responses to Con A and PHA. The latter inhibition observed following 6-12 months of exposure may be due to the in vivo generation of suppressor lymphocytes. Unfractionated lymphocytes from blood or alveolar space as well as enriched T cells from high dose exposed animals suppressed the proliferative responses of pulmonary or circulating lymphocytes to PHA and Con A, but not to PWM. Similarly, pre-incubation of normal blood or pulmonary lymphocytes in serum from high dose exposed animals for 24 h induced the appearance of suppressor cell activity in these populations when further tested in a co-culture assay with normal fresh lymphocytes. Taken together, these studies demonstrate the multi-faceted effects of asbestos on the immune system. The eventual fibrogenic process of asbestosis may result from the interplay of several mechanisms, some of which are suggested in this work.

• Asbestos exposure correlates with alterations in circulating T cell subsets. L.G. Miller, D. Sparrow, L.C. Ginns. 1983;51(1):110-6. PubMed · Free full text

  Abstract

  Peripheral blood lymphocytes were analysed from 40 subjects with occupational asbestos exposure and 40 controls matched for age and smoking habits. Patients were classified by duration of exposure as short or long, and by chest radiograph as normal, pleural plaques or interstitial changes. As a group, subjects with asbestos exposure had decreased percentages of OKT3+ and OKT8+ cells and increased OKT4+/OKT8+ ratio compared to controls. Correcting for age and smoking, those with short exposure were similar to controls, while those with long exposure had decreased percentages OKT3+ and OKT8+ cells and an increased OKT4+/OKT8+ ratio. Among radiographic subgroups, those with normal radiographs were similar to controls, but those with plaques had increased circulating OKT4+ cells, and those with interstitial changes had decreased percentages OKT3+ and OKT8+ cells and OKT8+ cells/mm3, with an increased OKT4+/OKT8+ ratio. There were no differences between subjects and controls in OKT10+ cells and OKIa+ cells. There appears to be a progressive decrease in percentage OKT8+ cells and increase in OKT4+/OKT8+ ratio with increasing exposure to asbestos, as determined by length of exposure and by radiographic abnormalities.

• In vitro suppression of fibroblast growth inhibitory lymphokine production by asbestos. I. Lemaire, C. Dubois. 1983;53(1):239-48. PubMed · Free full text

  Abstract

  Human peripheral blood mononuclear leucocytes (PBML) stimulated with concanavalin A (Con A) or phytohaemagglutinin (PHA) produced a soluble factor which inhibits lung fibroblast DNA synthesis and growth. Lymphocyte enriched preparations produced significant growth inhibitory activity in the presence of PHA whereas media from adherent mononuclear cells incubated in the presence of the mitogen did not contain similar activity. This fibroblast growth inhibitory factor (FGIF) was non-dialysable, heat stable and resistant to pH 5. FGIF was also resistant to treatment with chymotrypsin and phosphodiesterase but partially sensitive to treatment with trypsin. Interestingly, there was significant suppression of FGIF production by PBML cultured with PHA in the presence of low concentrations of chrysotile asbestos (5-25 micrograms/ml). In this regard, asbestos (25 micrograms/ml) was not cytotoxic for lymphocytes but had a damaging effect on monocytes as evidenced by the release of lactate dehydrogenase (LDH) a cytoplasmic enzyme, in their culture media. These findings indicate that stimulated lymphocytes have the ability to inhibit fibroblast proliferation by releasing FGIF and that asbestos interfere with this process. Thus, while FGIF may regulate the extent of connective tissue proliferation during normal repair process, suppression of its production by asbestos may contribute to excessive fibroblast accumulation and fibrosis.

• Asbestos related changes in pulmonary and systemic immune responses--early enhancement followed by inhibition. M. Rola-Pleszczynski, I. Lemaire, P. Sirois, et al. 1982;49(2):426-32. PubMed · Free full text

  Abstract

  We recently developed an animal model in order to study the pulmonary and systemic reactions following exposure to environmental pollutants. In this model, conscious sheep received repeated intratracheal instillations of a suspension of 0 (controls), 2mg (low dose) or 128 mg (high dose) of chrysotile asbestos fibres over a 12 month period. A significant dose-dependent enhancement in proliferative responses of pulmonary free airway cells (FAC) to four mitogens was observed after a first instillation. A somewhat weaker stimulation was also observed in peripheral blood mononuclear leucocytes (PBML). At 6 months, the high dose animals no longer displayed the dose-dependent enhancement of FAC responses and manifested actual depression of PBML responses. At 12 months, all asbestos exposed animals showed impaired responses of FAC, whereas only the PBML of high dose animals were showing such an impairment. These data suggest that asbestos exposure has a dose-dependent initial enhancement of local pulmonary as well as systemic responses to mitogens while prolonged exposure and higher doses can subsequently lead to a relative depression of local and systemic cellular immune activity. Although responsive early after asbestos exposure, systemic immunity appears to lag behind local immunity in the late depressive effect of asbestos fibres on mitogen responsiveness. In addition to these cell-directed effects serum factors seem to play an inhibitory role in lymphocyte responses to mitogens in animals repeatedly exposed to asbestos.

• In vitro depression of human lymphocyte mitogen response (phytohaemagglutinin) by asbestos fibres. R.G. Barbers, W.W. Shih, A. Saxon. 1982;48(3):602-10. PubMed · Free full text

  Abstract

  Asbestosis is a fibrotic lung disease associated with chronic inhalation of asbestos dust. The response of peripheral blood mononuclear cells (PBM) to phytohaemagglutinin (PHA) in asbestosis patients has been reported to be impaired, suggesting a disturbance in the cell-mediated response of chronically exposed individuals. We demonstrated that PHA responses of normal PBM are also depressed when exposed to various forms of asbestos fibres in vitro. Furthermore, we showed the primary effect of the fibres to be on lymphoid (non-adherent) populations rather than monocytes (adherent cells). Exposure as brief as 1 hr affected the subsequent PHA response of the cells. This effect did not appear to involve suppressor cell activation nor was it mediated by soluble factors. Our findings therefore offer an explanation for the alterations in the cellular immune response observed in humans as a result of lymphoid cells coming into transient contact with inhaled asbestos fibres residing in the lung.

• Diminished suppressor cell function in patients with asbestosis. H.R. Gaumer, N.J. Doll, J. Kaimal, et al. 1981;44(1):108-16. PubMed · Free full text

  Abstract

  Epidemiological and immunological studies of asbestos workers documented abnormalities in humoral and cell-mediated immunity which could result from defective immunoregulation. This study tests this hypothesis with comparison of lymphocyte function in age-, sex- and smoking-matched subjects with asbestosis. In vivo measure of delayed hypersensitivity (i.e. skin test response) was significantly depressed to two recall antigens, SKSD and Candida, in asbestosis patients. Skin reaction to dinitrochlorobenzene (DNCB) was not depressed, although lymphocytes of patients giving positive skin test reactions demonstrated a significantly lower (P less than 0.001) proliferative response to dinitrobenzene sulphonic acid (DNBSO3) in vitro. T cell counts (E-rosettes) were normal in patients with asbestosis, although a subset of T cells, those forming sheep erythrocyte rosettes after prolonged incubation (Elate), were significantly depressed (P less than 0.003). This population has been equated with 'suppressor' cells (Grossi et al., 1978). Numbers of B cells were increased nearly two-fold over controls. Mitogen response of lymphocytes was normal except at suboptimal doses of mitogens where the response is known to be influenced by suppressor cell activity, which was significantly elevated. Suppressor cell function, as determined by stimulation of peripheral blood lymphocytes preincubated with concanavalin A, was also significantly decreased in asbestosis patients (P less than 0.01).

• Sequential immunological studies in an asbestos-exposed population. II. Factors affecting lymphocyte function. M.J. Campbell, M.M. Wagner, M.P. Scott, et al. 1980;39(1):176-82. PubMed · Free full text

  Abstract

  As part of an immunological study being carried out on a population exposed to asbestos the effect of two mitogens, phytohaemagglutinin (PHA) and pokeweed mitogen (PWM) on lymphocyte transformation has been assessed on three separate occasions for each mitogen. Both mitogens were assayed using foetal calf (FCS) or autologous serum (AS). Those men with pulmonary fibrosis (as measured by the presence of small opacities on X-ray) had a decrease (P less than 0.05) using PHA (FCS) when compared with those men with normal chest X-rays. Allowance has had to be made for the significant decline with age for both PHA (FCS and AS) transformation. There is a significant increase in PHA (FCS) and PWM (FCS) in ex-smokers and a further increase in smokers. These trends were consistent (at a lower level of significance) from survey to survey. There was no interaction between X-ray category and smoking. The lymphocyte antibody dependent cytotoxic test was measured on four occasions; the only observable effect was a non-significant increase in relation to smoking.

1970s

• Sequential immunological studies on an asbestos-exposed population. I. Factors affecting peripheral blood leucocytes and T lymphocytes. M.M. Wagner, M.J. Campbell, R.E. Edwards. 1979;38(2):323-31. PubMed · Free full text

  Abstract

  Peripheral blood leucocyte counts, and E binding rosettes were measured on 138 men on five separate occasions. Little effect was seen from age, or length of asbestos exposure. Overall the most marked effect was that obtained from smoking. Most relevant was an increase in percentage of E-rosettes read after 1 1/2 hrs, which was obtained in the group of those with radiological evidence of fibrosis who smoked. Restricted to subjects with small opacities, those who smoke have a significantly higher (P less than 0.05) percentage E 1 1/2 hr rosettes than those who do not smoke. (Percentage E rosettes read overnight remained unaltered by smoking or X-ray). This increase was found on each occasion that it was measured. Since the absolute number of T lymphocytes rosetting at 1 1/2 hr did not increase, it is suggested that there is either no stimulation of the central pool of T lymphocytes or a decrease in the absolute number of T lymphocytes which could only rosette overnight.

• Lymphocyte responses to phytohaemagglutinin in patients with asbestosis and pleural mesothelioma. P.L. Haslam, A. Lukoszek, J.A. Merchant, et al. 1978;31(2):178-88. PubMed · Free full text

  Abstract

  Quantitative impairment of lymphocyte responses to phytohaemagglutinin (PHA) has been demonstrated in six (21%) out of twenty-eight patients with asbestos-associated pulmonary fibrosis, in comparison with a group of unexposed normal controls. The impairment tended to occur in patients with fairly severe fibrosis, comparatively short duration of exposure to asbestos dust and with increases in serum immunoglobulin levels. One patient with asbestosis and an associated bronchial carcinoma also had depressed lymphocyte responses to PHA. These findings suggest a relationship between defective T-lymphocyte function and the fibrotic response in asbestosis. Whether it is also linked with the development of lung cancer, occurring either before or at a pre-clinical stage of tumour growth, and is of value in identifying patients especially at risk should now be explored in longitudinal studies. However, eight out of ten patients with asbestos-associated pleural mesothelioma and without lung fibrosis showed no evidence of impaired cellular immunity, either by in vitro testing with PHA or by vivo delayed hypersensitivity skin testing, indicating that impaired T-lymphocyte function is unlikely to be a common finding in all types of asbestos-associated malignancy.

• Immune adherence reactivity of rat alveolar macrophages following inhalation of crocidolite asbestos. K. Miller, E. Kagan. 1977;29(1):152-8. PubMed · Free full text

  Abstract

  The immune adherence phenomenon was used to demonstrate the in vivo deposition of complement on membranes of alveolar macrophages from rats chronically exposed to crocidolite asbestos dust. Pre-treatment of macrophage cualtures with anti-C3 antiserum greatly diminished the level of immune adherence reactivity. Alveolar macrophages exposed to crocidolite asbestos in vitro did not exhibit significant levels of immune adherence reactivity. These results may reflect an in-vivo antigen-antibody-complement interaction on the surface of a alveolar macrophages from animals which have inhaled asbestos dust.

• Immunological studies of patients with asbestosis. I. Studies of cell-mediated immunity. E. Kagan, A. Solomon, J.C. Cochrane, et al. 1977;28(2):261-7. PubMed · Free full text

  Abstract

  A variety of cancers have been documented in patients exposed to asbestos dust. Since a deranged immune system may play a rôle in cancer development, the general level of immunocompetence was studied in a group of twenty-six patients with radiographically defined asbestosis, who might be at risk of developing asbestos-related neoplasms. Statistical comparisons were made with a comparable control group. A disproportionate number of the patients displayed cutaneous energy to certain recall antigens and to 2,4-dinitrochlorobenzene. In vitro studies of cellular immunity, as evaluated by phytohaemagglutinin-induced proliferative and cytotoxicity assays, showed significantly lower values amongst the patient group. Serum inhibitors of mitogen-induced lymphocyte transformation were also detected in several of the patients. The possible significance of these findings is discussed.

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