Abstract
Identical cutaneous lesions can be elicited by several combinations of the following pathogens that in themselves are inactive and essentially different: (1) "sensitizers," which induce a latent predisposition for a specific reaction form (eg, inflammation, calcification, thrombosis and hemorrhage, necrosis); and (2) "challengers," which unmask this predisposition by making the disease manifest and determining its location. It may be significant that in all the disease models mentioned in this review, mast-cell dischargers and mast-cell products act as potent elicitors for diverse skin reactions; it therefore appears justified to conclude that close relationships exist between mast cells and tissue resistance to numerous pathogens.

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