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Figure 2: Ahr agonists suppress murine models of autoimmunity. Activation of Ahr by TCDD attenuates experimental autoimmune encephalomyelitis (EAE), ulcerative colitis (UC), experimental autoimmune uveoretinitis (EAU), and diabetes I by promoting differentiation of regulatory T cells (Tregs). With the exception of diabetes I, TCDD inhibits T helper (Th)-17, interferon (IFN)- , and interleukin (IL)-17. In EAE, Ahr signaling results in upregulation of transforming growth factor (TGF)- , IL-10, and acetylcholinesterase (AChE)-targeting microRNA (miR)-132. In addition to that mentioned above, TCDD downregulates tumor necrosis factor (TNF)- , monocyte chemotactic protein (MCP)-1, and keratinocyte chemoattractant (KC). Activation of Ahr by diindolylmethane (DIM) ameliorates EAE and UC by inducing Tregs and inhibiting proinflammatory cytokines including IFN- , IL-6, and tumor necrosis factor (TNF)- . Also, the DIM decreases inflammation in UC by inhibiting inducible nitric oxide synthase (iNOS) that produces nitric oxide (NO) and suppressing prostaglandin E2 (PGE2) by inhibiting COX-2, as well as inhibition of myeloperoxidase and nuclear factor (NF)- B activation. DIM treatment inhibits the expression of receptor activator for ligand (RANKL), leading to the blockade of osteoclastogenesis and consequently an alleviation of experimental arthritis. In addition, the DIM reduces IL-1 , TNF- , and NO in arthritis model.