EOSINOPHILS BIND RHINOVIRUS AND ACTIVATE VIRUS-SPECIFIC T-CELLS

Episodes of virus-induced exacerbations of asthma are accompanied by i ncreased eosinophils (EOS) in respiratory secretions and evidence of E OS degranulation, Although rhinoviruses (RV) are the viruses most ofte n implicated in exacerbations of asthma in both children and adults, l ittle is known about the immune response to this group of viruses and, in particular, EOS-RV interactions, To define such interactions, we i ncubated human rhinovirus type 16 (RV16), a serotype using ICAM-1 as a receptor, with EOS purified from PBMC, and measured EOS-RV binding, E OS-mediated Ag presentation and T cell activation, and EOS cell surfac e marker expression and superoxide production, Significant RV16 bindin g occurred to EOS that were pretreated with granulocyte-macrophage CSF , and this binding was inhibited by anti-ICAM-1 mAb, EOS also presente d viral Ags to RV16-specific T cells) causing T cell proliferation and secretion of IFN-gamma, RV16 induced a significant shift from CD18(di m) to CD18(bright), but did not affect EOS expression of CD54, CD69, o r HLA-DR, Finally, RV16 did not induce superoxide production from peri pheral blood EOS, These findings suggest that RV16 also binds to airwa y EOS, which resemble granulocyte-macrophage CSF-treated blood EOS in terms of high expression of ICAM-1, Furthermore, our findings suggest that EOS could participate in RV-induced immune responses through Ag p resentation and T cell activation, By activating RV-specific T cells, EOS may play an important role in the initiation of antiviral T cell r esponses, and these effects could also contribute to enhanced airway i nflammation and increased asthma symptoms in susceptible individuals.