<unk>  microscopically consists of dermal epithelioid histiocytes around a central zone of mucin—a so-called palisaded granuloma. Pathogenesis<unk>  is an idiopathic condition, though many catalysts have been proposed. Among these is skin trauma, UV exposure, vaccinations, tuberculin skin testing, and Borrelia and viral infections. The mechanisms proposed at a molecular level vary even more. In 1977, Dahl et al. proposed that since the lesions of<unk>  often display a thickening of, occlusion of, or other trauma to blood vessels, blood vessels may be responsible for<unk> . From their study of 58 patients, they found that immunoglobin M (IgM), complement, and fibrinogen were in the blood vessels of<unk>  areas, suggesting that<unk>  may share similarities with an immune-mediated, type 3 reaction or that chronic immune vasculitis may be involved in the pathogenesis. Another study found evidence suggesting blood vessel involvement with masses of intercellular fibrin and thickened basal lamina found around capillaries. Umbert et al. (1976), proposed an alternative pathogenesis: cell-mediated immunity. Their data suggests that lymphokines, such as macrophage-inhibiting factor (MIF), leads to sequestration of macrophages and histiocytes in the dermis. Then, upon lysosomal enzyme release by these sequestered cells, connective tissue damage ensues, which results in<unk> . Later, these authors found data suggesting that activation of macrophages and fibroblasts are involved in the pathogenesis of<unk>  and that fibrin and the rare IgM and C3 deposition around vessels were more likely a delayed-type hypersensitivity with resulting tissue and vessel changes rather than an immune-complex mediated disease. Further data has been collected supporting this finding.
Granuloma annulare
Ichthyosis bullosa of Siemens
Tuberculosis cutis orificialis
Generalized granuloma annulare
Aromaticum rosatum
Keratosis follicularis
Keratosis pilaris atrophicans
Tuberculosis verrucosa cutis