Dermatitis characterized by mastocytosis at immunization sites in mast-cell-deficient W/W^vmice

W/W^v mice have been extensively used as an important model to study the maturation/differentiation and pathophysiology of mast cells. These albino mice have been shown to have less than l%of the mast cells found in the skin of their +/+ controls or other normal mice. Morecwer, no mast cells are detected in other organs even though they apparently have an adequate number of mast cell precursors. Presumably, these precursons do not respond appropriately to microenvironmental growth factors, while ‘normal’ precursors from the +/+ controls ofSl/Sl^d-deficient mice mature appropriately in the tissue microenvironment of the W/W^v mice. Female W/W^v mice and +/+ controls were immunized with allogeneic spinal cord homogenate in complete Freund’s adjuvant and Mycobacterium tuberculosis in order to induce experimental allergic encephalomyelitis. All W/W^v mice developed extensive dermatitis with mastocytosis at the injection sites about 4 months after inoculation. Mast cells were identified by light microscopy following staining with toluidine blue and berbe- rine sulfate as well as electron microscopy. They were also found to be functional since they secreted serotonin and histamine in response to either compound 48/80 or carbachol. The majority of these mast cells were, therefore, considered to be mature, connective tissue like, but many of them were in different stages of granule maturation as seen with electron microscopy. These findings imply that W/W^v mice may not always be appropriate as models of mast cell deficiency. Moreover, these results suggest that the 'defect’ in W/W^v mast cell precursors can be overcome by factors produced during immunization and/or development of dermatitis. These findings may, therefore, help elucidate what regulates mast cell maturation/differentiation as well as their pathophysiology.