AuthOr’s VIew AuthOr’s VIew

In addition to the generation of protec-tive immune responses, effective immune defense strategies depend on intricate negative regulation to restrict tissue dam-age due to inflammation. Interleukin-10 (IL-10) is an immunosuppressive cyto-kine produced by and acting on many different leukocytes, including dendritic cells (DCs) and T cells.1,2 In particular, regulatory T cells (Tregs) exert their immunosuppressive function largely via the secretion of IL-10. As a gatekeeper of excessive immune responses against foreign antigens, IL-10 is expressed at epithelial interfaces to the environment, including the skin. Consequently, IL10−/− mice develop increased contact hyper-sensitivity (CHS),3 a relevant mouse model for allergic contact dermatitis.4 Following the topical application of a contact sensitizer (hapten), DCs prime hapten-specific T cells in skin-draining lymph nodes (sdLNs). The subsequent painting of the same hapten onto the ears triggers a transient ear-swelling reaction, driven by interferon γ (IFNγ)-secreting T H 1 cells and regulated by CD4+ T cells producing IL-10. Mice bearing a T cell-or Treg-specific deletion of IL10 exhibit aggravated CHS, demonstrating the essential role of T cell-derived IL-10 to curtail the inflammatory skin reaction.5,6 IL-10 control of dendritic cells in the skin Björn e. Clausen1,2, * and Mathilde J.h. Girard-Madoux