
SignificanceAhR, which is expressed in many epithelial, mucosal, and immune cells, represents a vital cellular sensor of environmental factors. Immune regulation by AhR can be cell, tissue, and ligand specific. Langerhans cells (LC), professional antigen presenting cells in the epidermis, govern the immunological barrier against environmental threats. How the AhR in LC regulates epicutaneous immune responses remains unclear. Experimenting with Langerin-specific AhR−/−mice, we discovered that AhR-deficient epidermal LC were reduced in number and, following epicutaneous protein (Ova) immunization, promoted T helper type-2 (Th2) and T regulatory type-1 (Tr1) responses, leading to increased Ova-specific IgE in the blood. Thus, AhR represents a critical sensor regulating LC activation and LC-mediated T cell polarization.
Ovalbumin, Mice, Transgenic, Immunoglobulin E, Administration, Cutaneous, T-Lymphocytes, Regulatory, Gene Knockout Techniques, Mice, Mannose-Binding Lectins, Th2 Cells, Receptors, Aryl Hydrocarbon, Langerhans Cells, Antigens, Surface, Basic Helix-Loop-Helix Transcription Factors, Animals, Lectins, C-Type, Epidermis
Ovalbumin, Mice, Transgenic, Immunoglobulin E, Administration, Cutaneous, T-Lymphocytes, Regulatory, Gene Knockout Techniques, Mice, Mannose-Binding Lectins, Th2 Cells, Receptors, Aryl Hydrocarbon, Langerhans Cells, Antigens, Surface, Basic Helix-Loop-Helix Transcription Factors, Animals, Lectins, C-Type, Epidermis
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