Virus-induced eosinophil mediator release requires antigen-presenting and CD4+ T cells.

摘要: Background The most frequent trigger of asthma exacerbation is infection with common airway viruses; however, the precise mechanism regulating such severe reactions not understood. presence eosinophil products a unique feature detected in asthmatic airways. Using an animal model, we previously demonstrated that T cells play important role eosinophil-dependant pathway virus-induced hyperreactivity. We hypothesize human eosinophils respond to viruses, although only after interaction cells. Objectives sought determine whether can viruses vitro and response. Methods An coculture model eosinophils, antigen-presenting cells, was used parainfluenza virus, respiratory syncytial or rhinovirus. measured release peroxidase (EPO) concert T-cell proliferation, cytokine release, changes phenotype. Results induced EPO when coincubated (dendritic macrophages) Virus-mediated associated proliferation CD3 + CD4 cytokines. UV inactivation virus did prevent proliferation. Proliferating show increased expression CD25 CD45RO. CD8 were activated. Conclusion Virus-induced occur context antigen presentation