| First Author | Croxford AL | Year | 2014 |
| Journal | J Invest Dermatol | Volume | 134 |
| Issue | 3 | Pages | 728-735 |
| PubMed ID | 24067382 | Mgi Jnum | J:206034 |
| Mgi Id | MGI:5547678 | Doi | 10.1038/jid.2013.404 |
| Citation | Croxford AL, et al. (2014) IL-6 Regulates Neutrophil Microabscess Formation in IL-17A-Driven Psoriasiform Lesions. J Invest Dermatol 134(3):728-35 |
| abstractText | The lack of a generally accepted animal model for human psoriasis has hindered progress with respect to understanding the pathogenesis of the disease. Here we present a model in which transgenic IL-17A expression is targeted to the skin in mice, achievable after crossing our IL-17A(ind) allele to the K14-Cre strain. K14-IL-17A(ind/+) mice invariably develop an overt skin inflammation bearing many hallmark characteristics of human psoriasis including dermal infiltration of effector T cells, formation of neutrophil microabscesses, and hyperkeratosis. IL-17A expression in the skin results in upregulated granulopoiesis and migration of IL-6R-expressing neutrophils into the skin. Neutralization of IL-6 signaling efficiently reduces the observed pathogenesis in skin of IL-17A-overexpressing mice, with marked reductions in epidermal neutrophil abscess formation and epidermal thickening. Thus, IL-6 functions downstream of IL-17A to exacerbate neutrophil microabscess development in psoriasiform lesions. |
