Hypothetical model of inflammatory LC differentiation. Epidermal keratinocytes express high levels of TSLP under inflammatory conditions. TGF-β1 is expressed by keratinocytes and was previously shown to promote LC differentiation. Martínez-Cingolani et al demonstrated that upon combined short-term stimulation with TSLP plus TGF-β1, human BDCA-1+ peripheral blood DCs acquire LC characteristics.1 They found that TSLP plus TGF-β1 synergistically promote LC differentiation from these cells. Whereas LCs undergo local proliferation in steady-state conditions, bone marrow–derived BDCA-1+ peripheral blood DCs may contribute to the pool of LCs during inflammation.

Hypothetical model of inflammatory LC differentiation. Epidermal keratinocytes express high levels of TSLP under inflammatory conditions. TGF-β1 is expressed by keratinocytes and was previously shown to promote LC differentiation. Martínez-Cingolani et al demonstrated that upon combined short-term stimulation with TSLP plus TGF-β1, human BDCA-1+ peripheral blood DCs acquire LC characteristics. They found that TSLP plus TGF-β1 synergistically promote LC differentiation from these cells. Whereas LCs undergo local proliferation in steady-state conditions, bone marrow–derived BDCA-1+ peripheral blood DCs may contribute to the pool of LCs during inflammation.

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