Psoriasis is a chronic inflammatory skin disease characterized by hyperplasia of the epidermis (acanthosis), infiltration of leukocytes into both the dermis and epidermis, and dilation and growth of blood vessels. The underlying cause of the epidermal acanthosis in psoriasis is still largely unknown. Recently, interleukin (IL)-23, a cytokine involved in the development of IL-17-producing T helper cells (T(H)17 cells), was found to have a potential function in the pathogenesis of psoriasis. Here we show that IL-22 is preferentially produced by T(H)17 cells and mediates the acanthosis induced by IL-23. We found that IL-23 or IL-6 can directly induce the production of IL-22 from both murine and human naive T cells. However, the production of IL-22 and IL-17 from T(H)17 cells is differentially regulated. Transforming growth factor-beta, although crucial for IL-17 production, actually inhibits IL-22 production. Furthermore, IL-22 mediates IL-23-induced acanthosis and dermal inflammation through the activation of Stat3 (signal transduction and activators of transcription 3) in vivo. Our results suggest that T(H)17 cells, through the production of both IL-22 and IL-17, might have essential functions in host defence and in the pathogenesis of autoimmune diseases such as psoriasis. IL-22, as an effector cytokine produced by T cells, mediates the crosstalk between the immune system and epithelial cells.

IL-19, IL-20, IL-22, IL-24, and IL-26 are members of the IL-10 family of cytokines that have been shown to be up-regulated in psoriatic skin. Contrary to IL-10, these cytokines signal using receptor complex R1 subunits that are preferentially expressed on cells of epithelial origin; thus, we henceforth refer to them as the IL-20 subfamily cytokines. In this study, we show that primary human keratinocytes (KCs) express receptors for these cytokines and that IL-19, IL-20, IL-22, and IL-24 induce acanthosis in reconstituted human epidermis (RHE) in a dose-dependent manner. These cytokines also induce expression of the psoriasisassociated protein S100A7 and keratin 16 in RHE and cause persistent activation of Stat3 with nuclear localization. IL-22 had the most pronounced effects on KC proliferation and on the differentiation of KCs in RHE, inducing a decrease in the granular cell layer (hypogranulosis). Furthermore, gene expression analysis performed on cultured RHE treated with these cytokines showed that IL-19, IL-20, IL-22, and IL-24 regulate many of these same genes to variable degrees, inducing a gene expression profile consistent with inflammatory responses, wound healing re-epithelialization, and altered differentiation. Many of these genes have also been found to be up-regulated in psoriatic skin, including several chemokines, ␤-defensins, S100 family proteins, and kallikreins. These results confirm that IL-20 subfamily cytokines are important regulators of epidermal KC biology with potentially pivotal roles in the immunopathology of psoriasis.

These results suggest that IL-19 plays a role in the complex pathological cytokine network in psoriasis.

Background and purposeCauda equina syndrome (CES) is a severe complication of lumbar spinal disorders; it results from compression of the nerve roots of the cauda equina. The purpose of this study was to evaluate the clinical usefulness of a classification scheme of CES based on factors including clinical symptoms, imaging signs, and electrophysiological findings.MethodsThe records of 39 patients with CES were divided into 4 groups based on clinical features as follows. Group 1 (preclinical): low back pain with only bulbocavernosus reflex and ischiocavernosus reflex abnormalities. Group 2 (early): saddle sensory disturbance and bilateral sciatica. Group 3 (middle): saddle sensory disturbance, bowel or bladder dysfunction, motor weakness of the lower extremity, and reduced sexual function. Group 4 (late): absence of saddle sensation and sexual function in addition to uncontrolled bowel function. The outcome including radiographic and electrophysiological findings was compared between groups.ResultsThe main clinical manifestations of CES included bilateral saddle sensory disturbance, and bowel, bladder, and sexual dysfunction. The clinical symptoms of patients with multiple-segment canal stenosis identified radiographically were more severe than those of patients with single-segment stenosis. BCR and ICR improved in groups 1 and 2 after surgery, but no change was noted for groups 3 and 4.InterpretationWe conclude that bilateral radiculopathy or sciatica are early stages of CES and indicate a high risk of development of advanced CES. Electrophysiological abnormalities and reduced saddle sensation are indices of early diagnosis. Patients at the preclinical and early stages have better functional recovery than patients in later stages after surgical decompression.

Study Design. This study is a systematic literature review and meta-analysis. Objective. To evaluate the efficacy of tubular microdiscectomy (TMD) compared with conventional microdiscectomy (CMD) for lumbar disc herniation (LDH). Summary of Background Data. TMD has developed rapidly due to reduced tissue trauma by minimization of the required access to spine and disc herniation; however, CMD remains the standard of care for this patient group. To date, it remains debatable whether TMD is superior to CMD for LDH. Methods. We performed a comprehensive database search of PubMed, EMBASE, and Cochrane Central Register of Controlled Trails for prospective randomized controlled trials (RCTs), through using Medical Subject Headings (MeSH) terms “microdiscectomy,” “tubular microdiscectomy,” “minimally invasive surgery,” and “spinal disease.” The retrieved results were last updated on March 15, 2018. Two independent investigators selected qualified studies, extracted indispensable data, assessed risk of bias of original papers. The Grades of Recommendation, Assessment, Development and Evaluation (GRADE) approach was used to grade quality of evidence. If I 2 >50, the heterogeneity is considerable. Results. Four RCT studies (total n = 605), involving 610 individuals with a follow-up period of no less than 12 months, were selected for further review. We assessed these studies as low overall risk of bias. There was low-quality evidence that TMD was superior to CMD considering postoperative Oswestry Disability Index scores (SMD, –3.43, 95% CI, –4.64 to –2.21, P < 0.00001). Compared with CMD, the TMD group exhibited significantly worse Short Form-36 physical function scores (SMD, –4.83, 95% CI, –8.94 to –0.72, P = 0.02). There were no significant differences in the visual analogue scale (P = 0.30), operative time (P = 0.68), dural tear (P = 0.52), and reoperation (P = 0.98). Conclusion. The benefits 1 year after TMD were similar to that of CMD. There was no significant difference in the incidence of reoperation and dural tear. Level of Evidence: 1