• William Damsky, Durga Thakral, Nkiruka Emeagwali, Anjela Galan, and Brett King.
• From the Departments of Dermatology (W.D., D.T., A.G., B.K.), Immunobiology (W.D.), and Pathology (A.G.) and the Department of Internal Medicine, Section of Pulmonary, Critical Care, and Sleep Medicine (N.E.), Yale School of Medicine, New Haven, CT.
• N. Engl. J. Med. 2018 Dec 27; 379 (26): 2540-2546.

AbstractThere is evidence that Janus kinase (JAK)-signal transducer and activator of transcription (STAT) signaling plays a role in the pathogenesis of sarcoidosis. We treated a patient with cutaneous sarcoidosis with the JAK inhibitor tofacitinib; the patient had not previously had a response to medications and had not received systemic glucocorticoids. This treatment resulted in clinical and histologic remission of her skin disease. Sequencing of RNA and immunohistochemical examination of skin-lesion samples obtained from the patient before and during therapy and immunohistochemical testing of lesion samples obtained from other patients with cutaneous sarcoidosis support a role for JAK-STAT signaling in cutaneous sarcoidosis. (Funded by the Ranjini and Ajay Poddar Resource Fund for Dermatologic Diseases Research and others.).

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