ABSTRACT
Inflammatory disorders that affect the skin are distinguished histologically by the nature, degree, and microscopic localization of leukocytes, often resulting in a distinctive clinical picture. Cutaneous neoplasms may also have leukocytic infiltrates that help to identify them histologically, such as the plasma cells that aid in the identification of syringocystadenoma papilliferum. The exact mechanisms responsible for the influx of characteristic leukocytes in many inflammatory disorders of the skin are poorly understood. Inherent to mechanisms of cutaneous inflammation are factors responsible for leukocyte homing to sites of skin inflammation, including expression of specific cell adhesion molecules (CAMs) on skin microvessels and chemoattractant factors important to transvascular diapedesis. Secretagogues are substances that cause mast cells to release their mediators by a process termed degranulation, whereby membrane-bound cytoplasmic granules undergo rapid exocytosis. Mast cells from different body sites also respond differently to stimuli. The functional analogy in skin is the role that activated postcapillary venules may assume in cutaneous leukocyte influx.
