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Contact hypersensitivity (CH) has served as a useful model for investigating the allergen-specific immune responses of T cells and skin-associated antigen-presenting cells. We examined the distinct role between CD80 and CD86 on hapten-induced CH in both an induction and an effector phase. Intraperitoneal injection of mAb against CD86, but not CD80, 2 h before sensitization with epicutaneous application of dinitrofluorobenzene led to an almost complete inhibition of ear swelling, and histologically a marked reduction of edema, inflammatory polymorphonuclear cells and lymphocyte infiltration in the dermis. In contrast, the administration with either anti-CD80 or CD86 mAb 2 h before challenge partially inhibited CH reactions and a combination of both mAb did not improve the inhibitory effect. Although Langerhans cells (LC) expressing MHC class II were observed in both the epidermis and dermis 24 h after primary sensitization, CD86(+) LC were observed only in the subepidermal regions and CD80-bearing cells were not detected. Dendritic cells (DC) expressing both CD80 and CD86 were preferentially observed in the T cell areas of draining lymph nodes 24 h after challenge. The administration of anti-CD86 mAb in the induction phase prominently reduced the up-regulation of CD80 and CD86 on DC in the lymph nodes. The predominant role of CD86 was further supported by a marked reduction in proliferation of lymph node T cells against the sensitized hapten after the anti-CD86 treatment. These results suggest that CD86 plays a critical role in the initiation of primary immune responses in the skin, while CD80 and CD86 are not essential in the effector phase of CH reactions.

The differential role of CD86 and CD80 co-stimulatory molecules in the induction and the effector phases of contact hypersensitivity