Interleukin-4 receptor-Stat6 signaling in murine infections with a tissue-dwelling nematode parasite.

Abstract

Interleukin-4 (IL-4) has been shown to be crucial in parasite expulsion in several gastrointestinal nematode infection models. Data from both epidemiological studies with humans and experimental infections in animals imply a critical role for the type II helper response, dominated by IL-4, in host protection. Here we utilized inbred mice on two distinct backgrounds to document the involvement of IL-4 in the clearance of a primary infection of Brugia from the murine host. Our data from infections of IL-4 receptor(-/-) and Stat6(-/-) mice further indicate that IL-4 exerts its effects by activating the Stat6 molecule in host target cells, a finding which links clearance requirements of a gastrointestinal tract-dwelling nematode with those of a tissue-dwelling nematode. Additionally, we show that the requirements for IL-4 receptor binding and Stat6 activation extend to accelerated clearance of a secondary infection as well. The data shown here, including analysis of cell populations at the site of infection and infection of immunoglobulin E (IgE)(-/-) mice, lead us to suggest that deficiencies in eosinophil recruitment and isotype switching to IgE production may be at least partially responsible for slower parasite clearance in the absence of IL-4.

• Authors: L Spencer, L Shultz, T V Rajan
• Journal: Infection and immunity (Infect Immun) Vol. 69 Issue 12 Pg. 7743-52 (Dec 2001) ISSN: 0019-9567 [Print] United States
• PMID: 11705956 (Publication Type: Journal Article, Research Support, U.S. Gov't, P.H.S.)

Chemical References

• Receptors, Interleukin-4
• STAT6 Transcription Factor
• Stat6 protein, mouse
• Trans-Activators
• Interleukin-4
• Immunoglobulin E

Topics

• Animals
• Brugia malayi
• Eosinophils (immunology)
• Filariasis (immunology)
• Host-Parasite Interactions
• Immunity, Innate
• Immunoglobulin Class Switching
• Immunoglobulin E (biosynthesis)
• Interleukin-4 (pharmacology)
• Mice
• Mice, Inbred BALB C
• Mice, Inbred C57BL
• Mice, Mutant Strains
• Mice, SCID
• Peritoneal Cavity (parasitology)
• Receptors, Interleukin-4 (genetics, metabolism)
• STAT6 Transcription Factor
• Signal Transduction
• Th2 Cells
• Trans-Activators (genetics, metabolism)