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Unité de Recherche, Centre de Pneumologie, Hôpital Laval, and Institut de Cardiologie et de Pneumologie, Université Laval, Ste Foy, Quebec, Canada.
Hypersensitivity pneumonitis (HP) is characterized by an influx of
activated T cells in the lungs. The CD28/B7 system provides
costimulatory signals essential for complete T cell activation and
differentiation. We have previously demonstrated that alveolar
macrophages from patients with HP have an up-regulated expression of B7
molecules. In the present study, we investigated the effect of i.p.
administration of CTLA4-Ig, a CD28/B7 antagonist, on the lung
inflammation of mice inoculated with Saccharoplyspora
rectivirgula (SR), a major causative agent of HP. Five groups
of C57BL/6 mice were intranasally instilled with SR or saline for 3
consecutive days per wk during 3 wk. CTLA4-Ig was administered starting
either after 1 wk of SR challenge or 6 h before the first
antigenic exposure and continued during the whole period of
sensitization. A control-IgG was given similarly during the 3 wk of SR
exposure. The groups included: 1, saline; 2, SR; 3, SR + control-Ig; 4,
SR + CTLA4-Ig for the last 2 wk; and 5, SR + CTLA4-Ig for 3 wk.
CTLA4-Ig treatment markedly decreased lung inflammation as shown by
significantly fewer inflammatory cells in the bronchoalveolar lavage
and in lung tissue and reduced SR-specific serum and bronchoalveolar
lavage Ig levels. Production of IL-4, IL-10, and IFN-
by
IL-2-stimulated pulmonary T cells was also decreased by CTLA4-Ig.
Administration of CTLA4-Ig did not affect the SR-induced up-regulation
of B7-2 expression. These results show that blockade of CD28/B7
interactions by CTLA4-Ig inhibits SR-induced lung inflammation and
immune response to SR Ag in mice and may provide a novel approach in
the treatment of HP.
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