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Although oxidative stress plays a major role in TCE-\/DCAC-mediated autoimmunity, the underlying molecular mechanisms still need to be delineated. Nuclear factor (erythroid-derived 2)-like2 (Nrf2) is an oxidative stress-responsive transcription factor that binds to antioxidant responsive element (ARE) and provides protection by regulating cytoprotective and antioxidant gene expression. However, the potential of Nrf2 in the regulation of TCE-\/DCAC-mediated autoimmunity is not known. This study thus focused on establishing the role of Nrf2 and consequent inflammatory responses in TCE-\/DCAC-mediated autoimmunity. To achieve this, we pretreated Kupffer cells (KCs) or T cells with\/without tert-butylhydroquinone (tBHQ) followed by treatment with DCAC. In both KCs and T cells, DCAC treatment significantly downregulated Nrf2 and HO-1 expression along with induction of Keap-1 and caspase-3, NF-\u03baB (p65), TNF-\u03b1, and iNOS, whereas pretreatment of these cells with tBHQ attenuated these responses. The in vitro findings were further verified in vivo by treating female MRL+\/+ mice with TCE along with\/without sulforaphane. TCE exposure in mice also led to reduction in Nrf2 and HO-1 but increased phospho-NF-\u03baB (p-p65) and iNOS along with increased anti-dsDNA antibodies. Interestingly, sulforaphane treatment led to amelioration of TCE-mediated effects, resulting in Nrf2 activation and reduction in inflammatory and autoimmune responses. Our results show that TCE\/DCAC mediates an impairment in Nrf2 regulation. Attenuation of TCE-mediated autoimmunity via activation of Nrf2 supports that antioxidants sulforaphane\/tBHQ could be potential therapeutic agents for autoimmune diseases.<\/jats:p>","DOI":"10.1093\/toxsci\/kfaa022","type":"journal-article","created":{"date-parts":[[2020,2,13]],"date-time":"2020-02-13T20:11:18Z","timestamp":1581624678000},"page":"64-74","source":"Crossref","is-referenced-by-count":24,"title":["Enhancing the Nrf2 Antioxidant Signaling Provides Protection Against Trichloroethene-mediated Inflammation and Autoimmune Response"],"prefix":"10.1093","volume":"175","author":[{"given":"Nivedita","family":"Banerjee","sequence":"first","affiliation":[{"name":"Department of Pathology, University of Texas Medical Branch, Galveston, Texas 77555-0438"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Hui","family":"Wang","sequence":"first","affiliation":[{"name":"Department of Pathology, University of Texas Medical Branch, Galveston, Texas 77555-0438"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Gangduo","family":"Wang","sequence":"first","affiliation":[{"name":"Department of Pathology, University of Texas Medical Branch, Galveston, Texas 77555-0438"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"M Firoze","family":"Khan","sequence":"first","affiliation":[{"name":"Department of Pathology, University of Texas Medical Branch, Galveston, Texas 77555-0438"}],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"286","published-online":{"date-parts":[[2020,2,19]]},"reference":[{"key":"2020050414174974800_kfaa022-B1","doi-asserted-by":"crossref","first-page":"585","DOI":"10.1016\/j.bbadis.2016.11.005","article-title":"Nrf2 signaling pathway: Pivotal roles in inflammation","volume":"1863","author":"Ahmed","year":"2017","journal-title":"Biochim. 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