| First Author | Suwanpradid J | Year | 2017 |
| Journal | J Immunol | Volume | 199 |
| Issue | 5 | Pages | 1827-1834 |
| PubMed ID | 28747341 | Mgi Jnum | J:251268 |
| Mgi Id | MGI:6099176 | Doi | 10.4049/jimmunol.1700739 |
| Citation | Suwanpradid J, et al. (2017) Arginase1 Deficiency in Monocytes/Macrophages Upregulates Inducible Nitric Oxide Synthase To Promote Cutaneous Contact Hypersensitivity. J Immunol 199(5):1827-1834 |
| abstractText | The innate immune components that modulate allergic contact hypersensitivity (CHS) responses are poorly defined. Using human skin from contact dermatitis patients and a mouse model of CHS, we find that hapten allergens disrupt the Arginase1 (Arg1) and inducible NO synthase (iNOS) dynamic in monocytes/macrophages (mono/MPhi), which renders those cells ineffectual in suppressing skin inflammation. Mice lacking Arg1 in MPhi develop increased CHS characterized by elevated ear thickening, mono/MPhi-dominated dermal inflammation, and increased iNOS and IL-6 expression compared with control mice. Treatment of Arg1(flox/flox); LysMCre(+/-) mice with a selective NOS inhibitor or knockout of Nos2, encoding iNOS, significantly ameliorates CHS. Our findings suggest a critical role for Arg1 in mono/MPhi in suppressing CHS through dampening Nos2 expression. These results support that increasing Arg1 may be a potential therapeutic avenue in treating allergic contact dermatitis. |
