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Volume 20 Issue 9, September 2014

Alopecia areata is an autoimmune disease characterized by immune-mediated attack of the hair follicle and hair loss. In this issue, Xing et al. find that cytotoxic T cells are necessary and sufficient for the development of alopecia areata in mice. Inhibition of interferon and common gamma chain cytokines or administration of JAK inhibitors prevent the development of disease, whereas JAK inhibitors promote hair regrowth in patients and mice with established disease. The cover image depicts IL-15 (green), IL-15 receptor α (red) and nuclei (DAPI, blue) in a skin resident-hair bulb from a patient with alopecia areata. Image courtesy of the Christiano and Clynes laboratories, Columbia University.

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  • The size, speed and potential reach of the 2014 Ebola virus outbreak in West Africa presents a wake-up call to the research and pharmaceutical communities—and to federal governments—of the continuing need to invest resources in the study and cure of emerging infectious diseases.

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  • Disrupted differentiation of Schwann cells contributes to axonal loss in a rat model of Charcot-Marie-Tooth 1A neuropathy. Early neuregulin-1 treatment promotes Schwann cell differentiation, preserves axons and restores nerve function in this model.

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  • Mutations in the DMD gene, encoding dystrophin, cause the most common forms of muscular dystrophy. A new study shows that forcing translation of DMD from an internal ribosome entry site can alleviate Duchenne muscular dystrophy symptoms in a mouse model.

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    • Kathryn N North
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  • Alopecia areata is an immune-mediated, nonscarring form of hair loss. A new study using human clinical samples and a mouse model demonstrates that CD8αβ+NKG2D+ T effector memory cells mediate alopecia areata in part through Janus kinase (JAK) signaling and that alopecia areata might be treated with JAK inhibitors.

    • Sherrie J Divito
    • Thomas S Kupper
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