Abstract:
UVB irradiation (290–320nm) is used to treat skin diseases like psoriasis and atopic dermatitis, and is known to
suppress contact hypersensitivity (CHS) reactions in mouse models. Regulatory T cells (Treg cells) have been
shown to be responsible for this UVB-induced suppression of CHS. The epidermal growth factor (EGF)-like
growth factor amphiregulin (AREG) engages EGFR on Treg cells and, in different disease models, it was shown that
mast cell–derived AREG is essential for optimal Treg cell function in vivo. Here we determined whether AREG has a
role in UVB-induced, Treg cell–mediated suppression of CHS reactions in the skin. Our data show that AREG is
essential for UVB-induced CHS suppression. In contrast to the general assumption, however, mast cells were
dispensable for UVB-induced immune suppression, whereas basophil-derived AREG was essential. These data
reveal, to our knowledge, a previously unreported function for basophils in the homeostasis of immune
responses in the skin. Basophils thus fulfill a dual function: they contribute to the initiation of effective type 2
immune responses and, by enhancing the suppressive capacity of local Treg cell populations, also to local immune
regulation in the skin.
