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Signals that regulate the host response to Mycobacterium tuberculosis
A D Beyers1, A van Rie, J Adams
1MRC Centre for Molecular and Cellular Biology, Faculty of Medicine, University of Stellenbosch, Tygerberg, South Africa.
Novartis Foundation Symposium
|February 9, 1999
Summary
A strong T helper 1 immune response is crucial for fighting tuberculosis. This study suggests that a dominant T helper 2 response, indicated by high IgE levels, increases tuberculosis susceptibility.
Area of Science:
- Immunology
- Infectious Diseases
- Tuberculosis Research
Background:
- T helper (Th) 1 immune responses are essential for eliminating Mycobacterium tuberculosis.
- Factors influencing T cell polarization to Th1 or Th2 cytokine production include genetics, cytokines, antigen characteristics, antigen-presenting cells, costimulatory molecules, hormones, and age.
- Children's T cells produce less gamma-interferon, potentially explaining clinical differences in tuberculosis.
Purpose of the Study:
- To investigate the relationship between T helper 2 (Th2) immune responses and susceptibility to Mycobacterium tuberculosis.
- To explore the role of serum IgE levels as a marker for Th2 dominance and its correlation with tuberculosis incidence.
- To examine the impact of active tuberculosis on Th2 responses.
Main Methods:
- Review of factors regulating T cell polarization to Th1 or Th2.
- Correlation analysis of serum IgE levels (marker of Th2 response) with tuberculosis incidence in a high-incidence community.
- Observation of serum IgE levels in patients before and after active tuberculosis treatment.
Main Results:
- Serum IgE levels, indicating Th2 responses, correlate with tuberculosis incidence and socioeconomic deprivation in a high-incidence community.
- Individuals with prominent Th2 responses may be more susceptible to M. tuberculosis.
- Serum IgE levels decline in patients after active tuberculosis, suggesting tuberculosis down-regulates Th2 responses.
Conclusions:
- Th2 immune dominance, potentially induced by factors like intestinal parasites, may enhance susceptibility to tuberculosis.
- The findings suggest a complex interplay between Th1/Th2 immune balance and tuberculosis pathogenesis.
- Tuberculosis infection appears to modulate the host's immune response, specifically down-regulating Th2 activity.