PYRIDOXINE SUPPLEMENTATION PROTECTS MICE FROM SUPPRESSION OF CONTACT HYPERSENSITIVITY INDUCED BY 2-ACETYL-4-TETRAHYDROXYBUTYLIMIDAZOLE (THI), ULTRAVIOLET-B RADIATION (280-320-NM), OR CIS-UROCANIC ACID

Evidence exists implicating the epidermal ultraviolet B (UVB) photopro duct cis-urocanic acid as an immunogenic mediator of the systemic supp ression of T cell-mediated immunity by UVB exposure. Cis-urocanic acid appears to act via histamine receptor pathways, and histamine recepto r antagonists and other imidazole ring compounds may modify its immune suppressing action. A component of the food coloring substance ammoni a caramel, 2-acetyl-4-tetrahydroxybutylimidazole (THI), which is known to cause lymphopenia in rats, appears to suppress immunity by a simil ar pathway when the contact hypersensitivity reaction has been the imm une function assay in mice. The induction of lymphopenia in rats by TH I is inhibited by the vitamin pyridoxine. This study demonstrates that the suppression of contact hypersensitivity in mice by UVB radiation, cis-urocanic acid, or THI is strongly inhibited by supplemental pyrid oxine, fed at 30 mg/kg diet, in comparison with the normal diet, which supplies 7 mg pyridoxine/kg diet. These results suggest that pyridoxi ne competes with cis-urocanic acid and THI for the same binding site o r receptor, which we postulate to be a histamine-like T lymphocyte rec eptor, and that a role may exist for the control of photoimmunosuppres sion by this vitamin.