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Type 2 immune response associated with silicosis is not instrumental in the development of the disease

¹Unit of Industrial Toxicology and Occupational Medicine, Université catholique de Louvain, Belgium; ²Division of Immunology, Institute of Infectious Disease & Molecular Medicine, Faculty of Health Science, University of Cape Town, South Africa; and ³Laboratory of Pathology, University Hospital of Mont-Godinne, Yvoir, Belgium

Submitted 29 November 2005 ; accepted in final form 6 July 2006

It has been proposed that the development of lung fibrosis is associated with a T helper type 2 response, mainly characterized by IL-4 and IL-13 production. We investigated the potential role of type 2 immune polarization in the silicotic process and examined the pulmonary response to silica particles in mice genetically deficient for IL-4. We found that IL-4^–/– mice were not protected against the development of silicosis, suggesting that IL-4 is not essential for the development of this fibrotic disease. By evaluating the intensity of silica-induced lung fibrosis in mice deficient for IL-4 receptor (IL-4R), we showed that the establishment of pulmonary fibrosis was independent of both IL-4 and IL-13. Strong impairment of the type 2 immune response (IgG₁) in the lungs of IL-4^–/– and IL-4R^–/– mice did not affect the development of the disease. Measurement of IL-132 receptor expression and IgG_2a, IL-12p70, and IFN- levels in silica-treated IL-4^–/– and IL-4R^–/– animals showed that the development of silicosis was not related to an IL-13 signaling pathway or a switch to a type 1 response in deficient animals. Our data clearly indicate that the type 2 immune response associated with silicosis in mice is not required for the development of this inflammatory and fibrotic disease.

inflammation; T helper type 2; lung fibrosis; cytokines

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