Gregory DeKrey PhD.

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The aryl hydrocarbon receptor is a ligand-activated transcription factor of the Per-Arnt-Sim (PAS) family of proteins that regulates cellular functions including immunity. It has been shown that 2,3,7,8-Tetrachlorodibenzodioxin (TCDD), a high affinity ligand for the aryl hydrocarbon receptor (AhR), suppresses immune responses in mice. AhR activation prior to immunization with cholera toxin results in suppression of anti-cholera toxin antibody responses. This is observed as lower immunoglobulin (IgA) levels in both feces and serum 14 days after immunization. Thereafter, cholera toxin (CT)-specific IgA fecal responses recover, where serum CT-specific antibody levels do not; something unexplained by the current paradigm for AhR regulation of immune responses. Because the half-life of TCDD in mice is approximately 7 days, immunosuppressive TCDD levels can persist for multiple weeks. It is unknown if a high dose of TCDD is necessary for the suppression of the fecal IgA response or if lower doses can achieve the same outcome in both feces and serum. The question is: does activation of the aryl hydrocarbon receptor via weekly, low dose exposure to TCDD cause altered IgA/IgG responses equivalent to that observed following a single, high dose exposure? The pertinence of this experiment is to better explain how the aryl hydrocarbon receptor exerts a modifying influence in different body compartments and how the homeostatic pattern of the AhR is related; giving a better understanding of how it may be exploited clinically. This question will be addressed through lab-based experimentation model outlines provided, using female C57B1/6 mice. Data were collected from immunologically relevant tissues (serum) and feces to ultimately determine levels of IgA and IgG.

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