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For more information visit www.uptodate.com.) Increasing amounts of evidence support autoimmune-mediated inflammation early in the course of morphea.14 Early morphea lesions are characterized by the influx of large amounts of mononuclear lymphocytes (usually activated T lymphocytes), plasma cells, and eosinophils.15 This is likely the result of autoimmunity, as there is widespread autoimmune reactivity in morphea patients (elevated ANAs, cytokines, and adhesion molecules).5,12,16 Morphea patients also have concomitant autoimmune disease at higher expected frequency than a healthy population.5,11 Vessel damage and upregulation of adhesion molecules (ICAM-1, VCAM 1, and E-selectin) occur related to the inflammatory cell infiltrate which facilitates local monocyte recruitment.17 These adhesion molecules are upregulated by cytokines classically associated with a Th2 immune response (Il-4, Il-1, and TNFs)