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Within the United States, foodborne diseases are estimated to result in more than 100,000 hospitalizations each year with 3,000 fatalities. Acute gastroenteritis impacts more than 1.5 million children each year in the United States. Worldwide, childhood morbidity and mortality are largely attributed to infectious diarrheal diseases. To combat infection at mucosal surfaces, immunoglobulin (Ig) A is produced by antibody-secreting B cells to inhibit and neutralize pathogens and their toxins. B cells are influenced by various extrinsic signals through activation of the aryl hydrocarbon receptor (AhR). The AhR is a ligand-activated transcription factor that links diet and environmental factors to intestinal immune function. Recently, some T cells have been shown to favor migration to the intestines after activation of the AhR in mice. B cell fate outcomes and antibody secretion are impacted by AhR activation, but it is unknown if B cell migration is also impacted. We have previously shown a decrease in IgA levels in serum of mice treated with the prototypic ligand for the AhR, 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD). In contrast, fecal IgA levels were unchanged by TCDD treatment. To explain this, we hypothesized that AhR activation favors migration of plasma cells out of blood-associated lymphoid tissues and into gut-associated lymphoid tissues through positively regulating the expression of molecules required for gut-homing. We predicted that the number of IgA-secreting cells in spleens would be significantly reduced by TCDD exposure in vivo and splenic B cells would have increased expression of gut migration markers when exposed to TCDD in vitro. To test this in vivo, we quantitatively determined IgA-secreting cells in the spleens of cholera toxin immunized mice. To elucidate the molecular mechanisms by which this differential regulation occurs in vitro, we exposed splenic CD19+ cells to AhR ligands for 96 hours, followed by flow cytometric analysis of expression of gut migration molecules. Treatment with TCDD in vivo significantly reduced the number of IgA-secreting cells contributing to systemic immunity and reduced the number of cholera toxin-specific IgA-secreting cells contributing to long-term systemic recall responses. Furthermore, AhR activity in vitro altered the expression of molecules required for gut-homing, suggesting that AhR activation in vivo positively regulates IgA-secreting cell trafficking to the small intestine. Because the gut contains approximately 80% of all antibody-secreting cells, secreting large quantities of IgA for defense against pathogenic infection and maintaining intestinal homeostasis, altering antibody-secreting cell migration is a promising target for the treatment of autoimmunity and the enhancement of intestinal disease resistance. The results of these studies fill a gap in knowledge regarding AhR modulation of gut antibody responses and expand our mechanistic understanding of how AhR activity influences intestinal disease resistance.