| First Author | Bromley SK | Year | 2013 |
| Journal | PLoS One | Volume | 8 |
| Issue | 3 | Pages | e58196 |
| PubMed ID | 23472158 | Mgi Jnum | J:199389 |
| Mgi Id | MGI:5502493 | Doi | 10.1371/journal.pone.0058196 |
| Citation | Bromley SK, et al. (2013) IL-23 induces atopic dermatitis-like inflammation instead of psoriasis-like inflammation in CCR2-deficient mice. PLoS One 8(3):e58196 |
| abstractText | Psoriasis is an immune-mediated chronic inflammatory skin disease, characterized by epidermal hyperplasia and infiltration of leukocytes into the dermis and epidermis. IL-23 is expressed in psoriatic skin, and IL-23 injected into the skin of mice produces IL-22-dependent dermal inflammation and acanthosis. The chemokine receptor CCR2 has been implicated in the pathogenesis of several inflammatory diseases, including psoriasis. CCR2-positive cells and the CCR2 ligand, CCL2 are abundant in psoriatic lesions. To examine the requirement of CCR2 in the development of IL-23-induced cutaneous inflammation, we injected the ears of wild-type (WT) and CCR2-deficient (CCR2(-/-)) mice with IL-23. CCR2(-/-) mice had increased ear swelling and epidermal thickening, which was correlated with increased cutaneous IL-4 levels and increased numbers of eosinophils within the skin. In addition, TSLP, a cytokine known to promote and amplify T helper cell type 2 (Th2) immune responses, was also increased within the inflamed skin of CCR2(-/-) mice. Our data suggest that increased levels of TSLP in CCR2(-/-) mice may contribute to the propensity of these mice to develop increased Th2-type immune responses. |
