Summary Interleukin (IL)-23 and CD4+ T helper-17 (Th17) cells are thought to be critical in the development of psoriasis. Here, we report that IL-23 predominantly stimulated dermal γδT cells to produce IL-17 that led to disease progression. Dermal γδT cells constitutively expressed the IL-23 receptor (IL-23R), RORγt, and various chemokine receptors. IL-17 production from dermal γδT cells was independent of αβT cells. The epidermal hyperplasia and inflammation induced by IL-23 were significantly decreased in T cell receptor δ deficient (Tcrd−/−) and IL-17 receptor deficient (Il17ra−/−) mice but occurred normally in Tcra−/− mice. Imiquimod-induced skin pathology was also significantly decreased in Tcrd−/− mice. Perhaps further promoting disease progression, IL-23 stimulated dermal γδT cell expansion. In psoriasis patients, γδT cells were also greatly increased in affected skin and produced large amounts of IL-17. Thus, IL-23-responsive dermal γδ T cells are the major IL-17 producers in the skin and may represent a novel target for the treatment of psoriasis.

On line 8, gd was wrong. It should've read ''.T cells was independent of ab T cells.'' On line 10, d was omitted. It should've read ''.significantly decreased in T cell receptor d-deficient.'' On line 12, Il17ra -/was wrong. It should've read ''.occurred normally in Tcra À/À mice.'' On line 14, Il17ra -/was wrong. It should've read ''.decreased in Tcrd À/À mice.''The authors are sorry for any confusion this may have caused.Additionally, the Note Added in Proof published with this paper online on October 6, 2011 contained the following sentence: ''After acceptance of this manuscript, two studies were published describing a similar population of dermal gd T cells.'' The sentence should've read: ''During review of this manuscript, two studies were published describing a similar population of dermal gd T cells.'' We apologize for any confusion this may have caused.

These data suggest that myonectin may be a useful marker in predicting the development of prediabetes and diabetes.

Cutaneous T cell lymphoma (CTCL) can have clinical and histological features resembling benign inflammatory dermatosis and can be difficult to diagnose. Very limited biomarkers are available for CTCL prognosis. We aimed to identify microRNA (miR) signatures to facilitate diagnostic and prognostic evaluations of CTCL. A cross-platform miR microarray identified 10 miRs that were differentially expressed between CTCL and benign inflammatory dermatosis patients. Subsequent reverse transcription polymerase chain reaction validation was used to generate a 5-miR-based diagnosing classifier, which showed high diagnostic accuracy in CTCL (area under the curve = 0.985 and 0.956 for training and testing set, respectively). Association between miR expressions and patient prognosis was studied. miR-155 and miR-200b were significantly associated with overall survival in CTCL patients, outperformed Ki-67. miR expressions were combined with Ki-67 to create a classifier for 5-year overall survival in CTCL patients. Our work provided miR signatures to facilitate CTCL diagnosis and prognosis with satisfying accuracy.

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BackgroundNanosecond pulsed electric fields (nsPEFs) can produce more significant biological effects than traditional electric fields and have thus attracted rising attention in developing medical applications based on short pulse duration and high field strength, such as effective cancer therapy. However, little is known about their effects on the differentiation of stem cells. Furthermore, mechanisms of electric fields on chondrogenic differentiation of mesenchymal stem cells (MSCs) remain elusive, and effects of electric fields on cartilage regeneration need to be verified in vivo. Here, we aimed to study the effects of nsPEFs on chondrogenic differentiation of MSCs in vitro and in vivo and further to explore the mechanisms behind the phenomenon.MethodsThe effects of nsPEF-preconditioning on chondrogenic differentiation of mesenchymal stem cells (MSCs) in vitro were evaluated using cell viability, gene expression, glycosaminoglycan (sGAG) content, and histological staining, as well as in vivo cartilage regeneration in osteochondral defects of rats. Signaling pathways were investigated with protein expression and gene expression, respectively.ResultsnsPEF-preconditioning with proper parameters (10 ns at 20 kV/cm, 100 ns at 10 kV/cm) significantly potentiated chondrogenic differentiation capacity of MSCs with upregulated cartilaginous gene expression and increased matrix deposition through activation of C-Jun NH2-terminal kinase (JNK) and cAMP-response element binding protein (CREB), followed by activation of downstream signal transducer and activator of transcription (STAT3). Implantation of nsPEF-preconditioned MSCs significantly enhanced cartilage regeneration in vivo, compared with implantation of non-nsPEF-preconditioned MSCs.ConclusionThis study demonstrates a unique approach of nsPEF treatment to potentiate the chondrogenic ability of MSCs through activation of JNK/CREB-STAT3 that could have translational potential for MSC-based cartilage regeneration.Electronic supplementary materialThe online version of this article (10.1186/s13287-019-1133-0) contains supplementary material, which is available to authorized users.