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in a Murine Model of Airway Inflammation: Expression of the IL-4 Receptor on Nonlymphoid Cells of Bone Marrow Origin Contributes to Severity of Inflammation1
Departments of
*
Immunology and
Pathology, Holland Laboratory, American Red Cross, Rockville, MD 20855; and
Department of Immunology, George Washington University Medical Center, Washington, D.C. 20037
Recent studies have suggested the IL-4R
expressed on lung epithelium is necessary for TH2-mediated goblet cell differentiation and mucus hypersecretion in a murine model of allergic lung disease. However, the IL-4R is expressed on numerous cell types that could contribute to the overall pathology and severity of asthma. The relative role of the receptor on these cells has not yet been conclusively delineated. To dissect the contribution of IL-4R in the development of pulmonary allergic responses, we generated murine radiation bone marrow (BM) chimeras. BM from IL-4R+ or IL-4R- mice was transferred into recipient mice that expressed or lacked IL-4R. In the absence of IL-4R in recipient mice, there was no goblet cell metaplasia or mucus hypersecretion in response to OVA, even in the presence of TH2 cells and substantial eosinophilic infiltration. More importantly, we found that expression of the IL-4R on a nonlymphoid, MHC class II+, BM-derived cell type contributes to the severity of inflammation and mucus production. These results suggest that IL-4 and IL-13 contribute to the development of allergic inflammation by stimulating a complex interaction between IL-4R+ cell types of both bone marrow and non-bone marrow origin.
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