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Meanwhile, Nrf2 can inhibit contact dermatitis through redox-dependent and -independent pathways. However, the underlying mechanisms of how Nrf2 mediates irritant contact dermatitis (ICD) are still unclear. In this article, we elucidated the role of Nrf2 in 12-O-tetradecanoylphorbol-13-acetate (TPA)-induced acute ICD. Our study demonstrated that the ear thickness, redness, swelling, and neutrophil infiltration were significantly increased, accompanied by increased expression of inflammatory cytokines (IL-1\u03b1, IL-1\u03b2, IL-6, etc.) and decreased expression of antioxidant genes (HO-1 and NQO1) in Nrf2 knockout mice. Moreover, ERK phosphorylation was elevated in mouse embryonic fibroblasts (MEFs) from Nrf2 knockout mouse. Inhibition of ERK significantly alleviated TPA-induced cutaneous inflammation and ROS accumulation in MEFs derived from mouse. Conversely, ROS scavenging inhibited the ERK activation and TPA-induced inflammation in MEFs. Taken together, the findings illustrate the key role of the Nrf2\/ROS\/ERK signaling pathway in TPA-induced acute ICD.<\/jats:p>","DOI":"10.4049\/jimmunol.2100577","type":"journal-article","created":{"date-parts":[[2022,2,23]],"date-time":"2022-02-23T17:50:32Z","timestamp":1645638632000},"page":"1424-1433","source":"Crossref","is-referenced-by-count":14,"title":["Aberrant HO-1\/NQO1\u2013Reactive Oxygen Species\u2013ERK Signaling Pathway Contributes to Aggravation of TPA-Induced Irritant Contact Dermatitis in Nrf2-Deficient Mice"],"prefix":"10.1093","volume":"208","author":[{"ORCID":"https:\/\/orcid.org\/0000-0003-0026-9934","authenticated-orcid":false,"given":"Junkai","family":"Huang","sequence":"first","affiliation":[{"name":"Immunology Department, Key Laboratory of Immune Microenvironment and Disease (Ministry of Education), Tianjin Medical University , Tianjin,","place":["China"]},{"name":"Department of Pathogen Biology and Immunology, Basic Medical College, Tianjin Medical 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