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The inverse association between tuberculin responses and atopic disorder
T Shirakawa1, T Enomoto, S Shimazu
1Lung Research Laboratory, Osler Chest Unit, Churchill Hospital, Oxford OX3 7LJ, UK. jhopkin@immsvr.jr2.ox.ac.uk
Science (New York, N.Y.)
|January 3, 1997
Summary
Exposure to Mycobacterium tuberculosis may protect against atopy and asthma. Positive tuberculin responses in schoolchildren were linked to lower asthma rates and reduced allergic sensitization, suggesting immune modulation.
Area of Science:
- Immunology
- Allergy Research
- Microbiology
Background:
- Human immune responses exhibit heterogeneity, with potential antagonism between T helper (TH) cell subsets and their associated cytokines.
- Atopy, characterized by immediate immunoglobulin E (IgE)-mediated hypersensitivity to allergens like dust mites and pollen, is a key factor in the rising prevalence of asthma.
Purpose of the Study:
- To investigate the association between delayed hypersensitivity to Mycobacterium tuberculosis and atopy in Japanese schoolchildren.
- To explore the potential immunomodulatory effects of M. tuberculosis exposure on allergic responses and asthma development.
Main Methods:
- Cross-sectional study involving Japanese schoolchildren.
- Assessment of delayed hypersensitivity using tuberculin skin testing.
- Measurement of serum immunoglobulin E (IgE) levels.
- Analysis of cytokine profiles to determine T helper cell bias (TH1 vs. TH2).
Main Results:
- A significant inverse association was observed between positive tuberculin responses and atopy.
- Children with positive tuberculin responses showed a lower incidence of asthma.
- Lower serum IgE levels were found in those with positive tuberculin responses.
- Cytokine profiles in this group were biased toward a TH1 type response.
Conclusions:
- Exposure to and immune response against Mycobacterium tuberculosis may inhibit the development of atopic disorders.
- The findings suggest that M. tuberculosis may modify immune profiles, offering a protective effect against atopy and asthma through mechanisms like TH1-biased immunity.