Abstract
Allergic rhinitis （AR） is a well-recognized chronic inflammatory disease of the nasal mucosa, being mainly mediated by antigen （Ag）-specific IgE and Th2-type T cell cytokines. The optimal activation of Ag-specific helper T cells is also well known to require the interaction of T cell receptors with Ag in the context of major histocompatibility complex （MHC） and also the involvement of appropriate co-stimulatory molecules. Moreover, although the interaction of CD28 and its ligands, CD80 and CD86, is known to play essential roles in the induction phase of AR as co-stimulatory pathways, the influence of such pathways on the development of the effector/ongoing phase of AR is still not fully understood. In the present study, the role of co-stimulatory pathways on the effector/ongoing phase of AR was studied using a murine model of AR. Intranasal administration of ovalbumin （OVA） elicited a strong Th2 immune responses. Following repeated nasal OVA challenge, the systemically presensitized BALB/c female mice developed significant Ag-induced nasal symptoms, nasal eosinophilia, serum levels of OVA-specific IgE and Th2-associated cytokines. Nasal administration of anti-CD86 antibody, but not anti-CD80 antibody, inhibited nasal symptoms, serum levels of OVA-specific IgE and IL-4 contents in nasal lavage fluids. In contrast, decrease in nasal eosinophilia and IL-5 levels in nasal lavage fluids were only observed in AR model mice, when they were treated with topical administration of both antibodies. These results demonstrated the importance of co-stimulatory pathways through the engagement of CD28 and CD86 in the development of the effector/ongoing phase of nasal inflammatory responses, especially AR.
