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Tofacitinib Treatment and Molecular Analysis of Cutaneous Sarcoidosis
Author(s) -
William Damsky,
Durga Thakral,
Nkiruka Emeagwali,
Anjela Galan,
Brett King
Publication year - 2018
Publication title -
new england journal of medicine
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 19.889
H-Index - 1030
eISSN - 1533-4406
pISSN - 0028-4793
DOI - 10.1056/nejmoa1805958
Subject(s) - tofacitinib , janus kinase , cutaneous sarcoidosis , medicine , sarcoidosis , stat protein , immunohistochemistry , janus kinase inhibitor , pathogenesis , lesion , dermatology , systemic disease , ruxolitinib , pathology , disease , immunology , signal transduction , cytokine , stat3 , rheumatoid arthritis , biology , bone marrow , biochemistry , myelofibrosis
There 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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