| First Author | Matsuo K | Year | 2021 |
| Journal | J Invest Dermatol | Volume | 141 |
| Issue | 8 | Pages | 1985-1994 |
| PubMed ID | 33662381 | Mgi Jnum | J:308541 |
| Mgi Id | MGI:6729776 | Doi | 10.1016/j.jid.2020.12.034 |
| Citation | Matsuo K, et al. (2021) CCR4 Involvement in the Expansion of T Helper Type 17 Cells in a Mouse Model of Psoriasis. J Invest Dermatol 141(8):1985-1994 |
| abstractText | Psoriasis is a chronic skin disease associated with T helper (Th)17-mediated inflammation. Because CCR4 is a major chemokine receptor expressed on Th17 cells, we investigated the role of CCR4 in a modified imiquimod-induced psoriasis model that showed enhanced skin infiltration of Th17 cells. CCR4-deficient mice had less severe skin disease than wild-type mice. Th17 cells were decreased in the skin lesions and regional lymph nodes of CCR4-deficient mice. In the regional lymph nodes of wild-type mice, CD44(+) memory Th17 cells expressing CCR4 were found to be clustered with dendritic cells expressing CCL22, a ligand for CCR4. Such dendritic cellTh17 cell clusters were significantly decreased in CCR4-deficient mice. Similar results were obtained using the IL-23induced psoriasis model. In vitro, compound 22, a CCR4 antagonist, significantly reduced the expansion of Th17 cells in the coculture of CD11c(+) dendritic cells and CD4(+) T cells separately prepared from the regional lymph nodes of wild-type mice with psoriasis. In vivo, compound 22 ameliorated the psoriasis-like skin disease in wild-type mice with significant decreases of Th17 cells in the regional lymph nodes and skin lesions. Collectively, CCR4 is likely to play a role in the pathogenesis of psoriasis through the expansion of Th17 cells. |
