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-Dependent Mechanism1
* Research Institute for Diseases of the Chest, Graduate School of Medical Sciences, Kyushu University, Fukuoka, Japan;
Department of Molecular Immunology, Graduate School, Tokyo Medical and Dental University, Tokyo, Japan;
Department of Internal Medicine 1, Kurume University School of Medicine, Kurume, Japan;
Department of Immunology, Juntendo University School of Medicine, Tokyo, Japan; and
¶
Sidney Kimmel Cancer Center, Johns Hopkins University School of Medicine, Baltimore, MD 21205
B7-H1 (PD-L1) and B7-DC (PD-L2) are the ligands for programmed death-1 (PD-1), which is a member of the CD28/CTLA-4 family and has been implicated in peripheral tolerance. We investigated the roles of B7-H1 and B7-DC in a murine OVA-induced allergic asthma model. B7-H1 was constitutively expressed on dendritic cells, macrophages, B cells, and T cells in the lungs of naive mice, and its expression could be dramatically increased after allergen challenge. In contrast, B7-DC expression was scarcely expressed on dendritic cells in naive mice, but was up-regulated after allergen challenge, although the up-regulation of B7-DC expression on macrophages was minimal. Treatment of mice with anti-B7-DC mAb at the time of allergen challenge, but not at the time of sensitization, significantly increased their airway hyper-reactivity and eosinophilia. Such treatment also resulted in the increased production of IL-5 and IL-13, and decreased IFN-
production in the lungs and draining lymph node cells. These changes were diminished when mice were depleted of IFN- by anti-IFN- mAb pretreatment. Interestingly, treatment with anti-B7-H1 or anti-PD-1 mAb did not significantly affect the asthmatic response. These results suggest a unique role for B7-DC in the regulation of asthmatic response through an IFN--dependent, but PD-1-independent, mechanism.
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