Diminished suppressor cell function in patients with asbestosis

Our plain-English summary of Diminished suppressor cell function in patients with asbestosis, by H.R. Gaumer, N.J. Doll, J. Kaimal, et al (Clinical and Experimental Immunology, 1981).

The study

• Authors: H.R. Gaumer, N.J. Doll, J. Kaimal, M. Schuyler, J.E. Salvaggio
• Journal: Clinical and Experimental Immunology
• Published: 1981;44(1):108-16
• Cited by: 38 articles, as counted by NIH iCite
• Read it: 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).

In plain English

This New Orleans study compared immune function in 10 men with asbestosis and matched healthy veterans without occupational asbestos exposure. Everyone in both groups smoked. Patients worked mainly in insulation, plumbing and cement work; the article does not say which fiber types they encountered. Fewer patients than controls reacted to skin tests with two familiar antigens (SKSD: 2 of 10 versus 7 of 10; Candida: 1 versus 6). Skin reactivity to a new chemical, DNCB, was not depressed. However, among those with positive DNCB skin tests, patients' lymphocytes responded less than controls' to the related compound DNBSO3 in the laboratory (6,361 versus 22,554 c.p.m.). Total T-cell counts were similar. 'Late' rosette-forming T cells, which the authors equate with suppressor cells, were significantly lower in patients; B cells were significantly higher. At the lowest doses of three stimulants, patients' cells responded much more. In a suppressor-cell test, mean inhibition was 20% for patients and 41% for controls. The authors concluded their data strongly favour decreased suppressor T-cell activity. They cautioned that most findings came from laboratory systems that may not reflect asbestos's action in the body.

We wrote this plain-English summary from the full article with the help of AI, and a second AI model checked each sentence against the article. It is not the authors' wording; the abstract and the article are their own account.

What the study did and found

• Design: Comparison of immune tests in asbestosis patients and matched control subjects (small clinical laboratory study)
• Who was studied: 10 male patients with asbestosis, aged 47 to 80, all cigarette smokers, studied at Tulane Medical School in New Orleans, Louisiana, USA. The 10 controls were healthy veterans undergoing routine physical examinations, with no occupational asbestos exposure, and all were smokers.
• Exposure: Occupational asbestos exposure in jobs such as insulation work, plumbing, cement manufacture, sanding machine work and asphalt labouring. Nine patients were exposed for 20 to 50 years, and one patient had 2 years of exposure mixing cement. The article does not state which fiber types these patients were exposed to. It mentions chrysotile only when discussing asbestos cytotoxicity in general and the authors' own laboratory experiments.
• Main results:
  • Positive skin tests to recall antigens were significantly fewer in patients (P less than 0.05). For SKSD, 2 of 10 patients and 7 of 10 controls were positive. For Candida, 1 of 10 patients and 6 of 10 controls were positive (counts from Table 2).
  • Skin reactivity to DNCB was not depressed in asbestosis patients. The text describes a trend toward greater reactivity in patients.
  • Among subjects with positive DNCB skin tests, patients' lymphocytes responded significantly less in the laboratory to DNBSO3 than controls' lymphocytes: 6,361 c.p.m. in patients versus 22,554 c.p.m. in controls.
  • At optimum and intermediate doses, responses to the mitogens PHA, PWM and Con A were similar in both groups. At the lowest doses, patients' cells responded more than controls' cells: PHA 1/100, 86,386 vs 38,222; PWM 1/200, 17,482 vs 2,989; Con A 5 micrograms/ml, 110,148 vs 9,384 c.p.m. (Table 4).
  • Total T cells (E rosettes) did not differ significantly between groups. 'Late' rosette-forming T cells (Elate), which the authors equate with suppressor cells, were significantly lower in patients (P less than 0.003).
  • B cell numbers were significantly elevated in asbestosis patients compared with controls (P less than 0.025).
  • In the Con A-induced suppressor cell assay, mean per cent inhibition of the Con A response was 20 (s.d. 32) in the 10 patients and 41 (s.d. 19) in the 10 controls (P less than 0.01). One patient (A.L.) showed 100% suppression.
• The authors' conclusion: The authors concluded that, although T cell numbers were normal, their data strongly favour decreased suppressor T cell activity in asbestosis patients. They hypothesized that altered T cell-B cell interaction may underlie the immune abnormalities.
• Limitations the authors state:
  • Most findings came from laboratory (in vitro) systems that may be too simplified to explain how asbestos acts in the body.
  • Too few patients had positive skin tests for a valid comparison of laboratory lymphocyte responses to the recall antigens.
  • The authors could not explain why patients had normal DNCB skin responses but lower laboratory responses to DNBSO3.
  • All subjects were heavy smokers. The authors suggest this might explain why their mitogen results differ from other studies.

Topics

The National Library of Medicine indexes this study under subjects our site covers: Asbestosis.

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