Infection of mice with Mycobacterium bovis-BCG induces both Th1 and Th2 immune responses in the absence of interferon-gamma signalling.

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

Infection of mice with Mycobacterium bovis-BCG induces both Th1 and Th2 immune responses in the absence of interferon-gamma signalling.

Eur Cytokine Netw. 1999 Jun;10(2):147-54. Unique Identifier : AIDSLINE MED/99328721
Erb KJ; Kirman J; Delahunt B; Moll H; Le Gros G; Zentrum fur Infektionsforschung, Universitat Wurzburg,; Rontgenring 11, 97070 Wurzburg, Germany.; zinf036@rzroe.uni-wuerzburg.de

Abstract: A murine pulmonary infection model using Mycobacterium bovis-BCG was used to study the development of Th1 and Th2 type responses in mice lacking a functional IFN-gamma receptor (IFN-gamma R-/-). Strikingly, the IFN-gamma R-/- mice maintained the Th1 response and developed a profound M. bovis-BCG, specific Th2 type immune response characterized by IL-5-producing CD4+ T cells, eosinophil infiltration of granulomas, and significantly elevated serum IgE levels. The increase in IL-5 production and eosinophil recruitment into the lung could be detected within the first 1-2 weeks of infection, indicating that the Th2 response was not due to greatly enhanced bacterial numbers observed later in infection. These results clearly indicate that IFN-gamma acts during M. bovis-BCG infection to suppress the development of Th2 immune responses. Furthermore, they demonstrate that IFN-gamma is not a necessary cofactor in the development of Th1 type cells secreting IFN-gamma. In conclusion, these data demonstrate that IFN-gamma plays a major role in suppressing a potentially disease-promoting Th2 immune response during mycobacterial infections.

Keywords: JOURNAL ARTICLE Animal Disease Models, Animal Eosinophilia/ETIOLOGY/PATHOLOGY Female IgE/BLOOD IgG/BLOOD Interferon Type II/*PHYSIOLOGY Lung/IMMUNOLOGY/PATHOLOGY Lymphokines/*SECRETION Male Mice Mice, Knockout Mycobacterium bovis/*IMMUNOLOGY/ISOLATION & PURIF Receptors, Interferon/DEFICIENCY/GENETICS Support, Non-U.S. Gov't Th1 Cells/*IMMUNOLOGY/SECRETION Th2 Cells/*IMMUNOLOGY/SECRETION Tuberculosis/BLOOD/*IMMUNOLOGY/MICROBIOLOGY Tuberculosis, Pulmonary/BLOOD/IMMUNOLOGY/MICROBIOLOGY
991130
A99B1067

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