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The Journal of Immunology, 2003, 170: 2037-2045.
Copyright © 2003 by The American Association of Immunologists

IL-13 Is Sufficient for Respiratory Syncytial Virus G Glycoprotein-Induced Eosinophilia After Respiratory Syncytial Virus Challenge 1

Teresa R. Johnson*,{dagger}, Robert A. Parker§, Joyce E. Johnson{ddagger} and Barney S. Graham2,*,{dagger}

* Vaccine Research Center, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD 20892; Departments of {dagger} Medicine and Microbiology and Immunology and {ddagger} Pathology, Vanderbilt University School of Medicine, Nashville, TN 37232; and § Department of Medicine (Biostatistics), Harvard University School of Medicine, Boston, MA 02115

Although well studied in settings of helminth infection and allergen sensitization, the combined contributions of IL-4 and IL-13 and their signaling pathways in models of viral pathogenesis have not been reported. Using a murine model of respiratory syncytial virus (RSV) infection, we evaluated the contribution of IL-13, alone and in conjunction with IL-4, during immunization with recombinant vaccinia virus expressing RSV G glycoprotein (vvGs) or with formalin-inactivated RSV (FI-RSV). We showed that both IL-4 and IL-13 activity must be inhibited to modulate G-specific responses resulting in severe RSV-induced disease. Inhibition of IL-4 or IL-13 activity alone had minimal impact on disease in vvGs-immunized mice. However, treatment of IL-4-deficient mice with IL-13Ra during vvGs immunization reduced IL-5, IL-13, and eotaxin production and pulmonary eosinophilia after RSV challenge. In contrast, FI-RSV-induced immune responses were diminished when either IL-4 or IL-13 activity was blocked. After RSV challenge, these type 2 T cell responses were also diminished in vvGs-primed IL-4R{alpha}-deficient mice. Our data suggest that secreted vvGs uses mechanisms requiring signaling through the IL-4R{alpha}-chain by either IL-4 or IL-13 for induction of eosinophilia and is the first description of the relative contributions of IL-4, IL-13, and their receptors in viral pathogenesis.




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