**1. Introduction**

The aryl hydrocarbon receptor (AhR) is a ligand-dependent transcription factor that mediates a variety of cellular events in many tissues [1]. AhR expression was found in many vertebrates such as rats and mice including fish. Therefore, it was suggested that AhR has a widespread biological function in animals, but its physiological role is not yet fully known. When AhR binds to xenobiotic ligands, the AhR regulates the expression of many genes including those encoding for cytochrome P450 enzymes. The activation of AhR was linked to variations in cell proliferation, apoptosis, tumor promotion, immune function, development, and reproductive functions [1, 2]. Many studies reported that the phenotype of AhRdeficient mice points to possible physiological functions of the receptor in liver, heart, ovary, vascular, and immune systems [2, 3]. The signaling pathway of AhR starts when AhR-ligand enters the responsive cell and binds with high affinity to the cytosolic AhR. The receptor exists as a multi-protein complex, containing two molecules of the chaperone heat shock protein of 90 kDa, the X-associated protein-2, and a 23-kDa co-chaperone protein [4]. The AhR undergoes conformational changes exposing a specific nuclear localization sequence which results

in the translocation of the complex into the nucleus [5]. The ligand:AhR will then be released from this complex and bind to a related nuclear protein called AhR nuclear translocator (ARNT), which converts the AhR into its high-affinity DNA-binding form [6]. The ligand:AhR:ARNT complex binds to its specific DNA recognition site, the dioxin response elements (DREs), resulting in stimulation of the transcription of cytochrome P450 (CYP1A1) and other AhR-responsive genes. Once the AhR-ligand binds to its receptor, the AhR:ligand complex will translocate into the nucleus. The ligand:AhR will then be released from this complex and bind to ARNT, which converts the AhR into its high-affinity DNAbinding form, and then the ligand:AhR:ARNT complex will bind to the DRE, and as a result, transcription of cytochrome P450 and other AhR-responsive genes will start.

The present chapter highlights the effects of some AhR-ligands both exogenous and endogenous, on the secretion of pro- and/or anti-inflammatory cytokines which control the production of different T helper cell subsets, and consequently affects inflammation, and autoimmunity.
