| First Author | Kim TG | Year | 2018 |
| Journal | J Invest Dermatol | Volume | 138 |
| Issue | 4 | Pages | 844-853 |
| PubMed ID | 29138056 | Mgi Jnum | J:261189 |
| Mgi Id | MGI:6154464 | Doi | 10.1016/j.jid.2017.11.003 |
| Citation | Kim TG, et al. (2018) Skin-Specific CD301b(+) Dermal Dendritic Cells Drive IL-17-Mediated Psoriasis-Like Immune Response in Mice. J Invest Dermatol 138(4):844-853 |
| abstractText | Conventional dendritic cells (cDCs) are composed of heterogeneous subsets commonly arising from dendritic cell (DC)-committed progenitors. A population of CD301b-expressing DCs has recently been identified in non-lymphoid barrier tissues such as skin. However, whether CD301b(+) DCs in the skin represent an ontogenetically unique subpopulation of migratory cDCs has not been fully addressed. Here, we demonstrated that CD301b(+) dermal DCs were distinct subpopulation of FMS-like tyrosine kinase 3 ligand (FLT3L)-dependent CD11b(+) cDC2 lineage, which required an additional GM-CSF cue for the adequate development. Although the majority of lymphoid-resident cDC2 lacked CD301b expression, dermal migratory cDC2 contained a substantial fraction of CD301b(+) subset. Similar to CD301b(-) population, CD301b(+) dermal DC development was closely regulated by FLT3 signaling, suggesting their common origin from FLT3L-responsive cDC progenitors. However, FLT3L-driven cDC progenitor culture was not sufficient, but additional GM-CSF treatment was required to produce CD301b(+) cDC2. In vivo development of CD301b(+) cDC2 was significantly augmented by exogenous GM-CSF, while the repopulation of CD301b(+) dermal cDC2 was abrogated by GM-CSF neutralization. Functionally, CD301b(+) cDC2 was capable of producing a high level of IL-23, and the depletion of CD301b(+) cDC2 effectively prevented IL-17-mediated psoriasiform dermatitis. Therefore, our findings highlight the differentiation program of a distinct CD301b(+) dermal cDC2 subset in the skin and its involvement in psoriatic inflammation. |
