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. doi: 10.1056/NEJMoa1805958.
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.).
有证据表明,Janus 激酶(JAK)-信号转导子和转录激活子(STAT)信号在结节病的发病机制中起作用。我们用 JAK 抑制剂托法替尼治疗了一名患有皮肤结节病的患者;该患者以前对药物没有反应,也没有接受过全身糖皮质激素治疗。这种治疗导致她的皮肤疾病临床和组织学缓解。对该患者在治疗前后获得的皮肤病变样本进行 RNA 测序和免疫组织化学检查,以及对其他患有皮肤结节病的患者的病变样本进行免疫组织化学检查,支持 JAK-STAT 信号在皮肤结节病中的作用。(由 Ranjini 和 Ajay Poddar 皮肤科疾病研究资源基金等资助)。