Second, several inflammatory mediators released during the immune response to H. pylori infection, such as IL-1, TNF-α, LTC4 and PAF, may play a role in the pathogenesis of urticaria lesions, at least in producing a nonspecific increase in sensitivity of the cutaneous vasculature to vasopermeability-enhancing agents [37]. The gene discussed is PCLAF; the disease is urticaria.