Contact hypersensitivity modulation

Kalergis, A.M., et al., Modulation of fatty acid oxidation alters contact hypersensitivity to urushiols Role of aliphatic chain B-oxidation in processing and activation of urushiols. Journal of Investigative Dermatology, 108, 57, 1997. 

It has been shown that, in an experimental granulomatous inflammation model, secretion of smCKBP by live e s modulated the diflerential recruitment of cells and the size of the egg granuloma, and it was proposed that smCKBP may facflitate granuloma formation and the propagation of the S. mansoni e s. Recombinant smCKBP suppressed inflammation induced in a mouse contact hypersensitivity model and inhibited CXCLS-induced pulmonary inflammation [66]. 

The suppression of T cell-mediated immunity by UV radiation appears to be a prerequisite for the outgrowth of UV-induced tumors in mice and is also manifested by an impaired ability to respond to contact sensitizing agents. Feeding AGE improved the impairment of contact hypersensitivity in hairless mice exposed to UVB (280-320 nm) radiation [41]. The modulation of UV-induced immunosuppression by AGE has been suggested to involve antagonism of the role of cis-urocanic acid, a natural photoproduct believed to participate as an immunogenic mediator. 

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