Signals that regulate the host response to Mycobacterium tuberculosis.

Important note: Information in this article was accurate in 1999. The state of the art may have changed since the publication date.

Signals that regulate the host response to Mycobacterium tuberculosis.

Novartis Found Symp. 1998;217:145-57; discussion 157-9. Unique Identifier : AIDSLINE MED/99134965
Beyers AD; van Rie A; Adams J; Fenhalls G; Gie R; Beyers N; MRC Centre for Molecular and Cellular Biology, Faculty of; Medicine, University of Stellenbosch, Tygerberg, South Africa.

Abstract: An appropriate T helper (Th) 1 immune response is required for the elimination of Mycobacterium tuberculosis. The factors regulating the polarization of mouse or human T cells to produce Th1 or Th2 cytokines are briefly reviewed. These factors include host genetics, cytokines present at the site of T cell activation, the type, dose and localization of antigen, the type of antigen-presenting cells, the engagement of different costimulatory molecules, steroid hormones and age. T cells of children produce low levels of gamma-interferon and we hypothesize that this may partly explain the differences in the clinical manifestations of tuberculosis in children and adults. Given that Th2 cytokines inhibit Th1 responses, the question arises of whether individuals mounting prominent Th2 responses, manifested by high serum IgE levels, are more susceptible to M. tuberculosis. In a community with a high incidence of tuberculosis, serum IgF levels, a marker of prominent Th2 responses, correlate with disease incidence and with socioeconomic deprivation. We propose that Th2 immune dominance, probably induced by intestinal parasites, enhances susceptibility to tuberculosis. Furthermore, our finding that serum IgE declines in patients following active tuberculosis argues that tuberculosis down-regulates Th2 responses.

Keywords: JOURNAL ARTICLE REVIEW REVIEW, TUTORIAL Age Factors Animal Cytokines/*IMMUNOLOGY Human Mice Receptors, Antigen, T-Cell/*IMMUNOLOGY Signal Transduction Support, Non-U.S. Gov't Th1 Cells/*IMMUNOLOGY Th2 Cells/*IMMUNOLOGY Tuberculosis, Pulmonary/EPIDEMIOLOGY/*IMMUNOLOGY
990530
A9950904

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