Jiaming Li, Zhaoyue Wang, Lan Dai, Lijuan Cao, Jian Su, Mingqing Zhu, Ziqiang Yu, Xia Bai, Changgeng Ruan
{"title":"Effects of rapamycin combined with low dose prednisone in patients with chronic immune thrombocytopenia.","authors":"Jiaming Li, Zhaoyue Wang, Lan Dai, Lijuan Cao, Jian Su, Mingqing Zhu, Ziqiang Yu, Xia Bai, Changgeng Ruan","doi":"10.1155/2013/548085","DOIUrl":"https://doi.org/10.1155/2013/548085","url":null,"abstract":"<p><p>We conducted this randomized trial to investigate the efficacy and safety of rapamycin treatment in adults with chronic immune thrombocytopenia (ITP). Eighty-eight patients were separated into the control (cyclosporine A plus prednisone) and experimental (rapamycin plus prednisone) groups. The CD4⁺CD25⁺CD127(low) regulatory T (Treg) cells level, Foxp3 mRNA expression, and the relevant cytokines levels were measured before and after treatment. The overall response (OR) was similar in both groups (experimental group versus control group: 58% versus 62%, P = 0.70). However, sustained response (SR) was more pronounced in the experimental group than in the control group (68% versus 39%, P < 0.05). Both groups showed similar incidence of adverse events (7% versus 11%, P = 0.51). As expected, the low pretreatment baseline level of Treg cells was seen in all patients (P < 0.001); however, the experimental group experienced a significant rise in Treg cell level, and there was a strong correlation between the levels of Treg cells and TGF-beta after the treatment. In addition, the upregulation maintained a stable level during the follow-up phase. Thus, rapamycin plus low dose prednisone could provide a new promising option for therapy of ITP.</p>","PeriodicalId":55254,"journal":{"name":"Clinical & Developmental Immunology","volume":"2013 ","pages":"548085"},"PeriodicalIF":0.0,"publicationDate":"2013-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1155/2013/548085","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"31976596","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"T cell vaccination inhibits Th1/Th17/Tfh frequencies and production of autoantibodies in collagen-induced arthritis.","authors":"Shan Li, Xiaoyin Niu, Yebin Xi, Shaohua Deng, Chengzhen Li, Qing Zhao, Guangjie Chen","doi":"10.1155/2013/967301","DOIUrl":"https://doi.org/10.1155/2013/967301","url":null,"abstract":"<p><p>The aim of this study is to determine whether the regulatory role of T cell vaccination (TCV) is through inhibition of Th1/Th17/Tfh and production of autoantibodies on collagen-induced arthritis (CIA). First, CIA mice were treated with TCV. After disease onset, the incidence and severity of change in joint histopathology were evaluated. Mice in the TCV-treated group showed less disease severity and less infiltration of inflammatory cells in the joint sections. TCV decreased the frequencies of Th1/Th17/Tfh cells and related cytokines. Reduction of IL-21 may be associated with both Tfh and Th17, which further influence B cell and T cell responses. In addition, inhibition of Th1/Th17/Tfh frequencies led to the reduced expression of T-bet, ROR α , ROR γ t, and Bcl6. Lastly, the proliferation of type-II-collagen-(CII-) specific T cells and the production of anti-CII antibodies were inhibited in the TCV-treated group. The results provide novel evidence that the therapeutic effects of TCV on CIA are associated with the inhibition of Th1/Th17/Tfh frequencies and autoantibodies production. </p>","PeriodicalId":55254,"journal":{"name":"Clinical & Developmental Immunology","volume":"2013 ","pages":"967301"},"PeriodicalIF":0.0,"publicationDate":"2013-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1155/2013/967301","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"31976598","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Dang Wu, Pin Wu, Qi Huang, Yang Liu, Jun Ye, Jian Huang
{"title":"Interleukin-17: a promoter in colorectal cancer progression.","authors":"Dang Wu, Pin Wu, Qi Huang, Yang Liu, Jun Ye, Jian Huang","doi":"10.1155/2013/436307","DOIUrl":"https://doi.org/10.1155/2013/436307","url":null,"abstract":"<p><p>It is widely accepted that chronic inflammation plays an active role in cancer. Inflammatory immunocytes and related cytokines in the tumor microenvironment are supposed to be a \"double-edged sword\" in colorectal cancer (CRC) initiation and progression. Interleukin-17 (IL-17), a pleiotropic proinflammatory cytokine, can promote cancer-elicited inflammation and prevent cancer cells from immune surveillance. Despite controversy, IL-17 is generally considered to be a promoter in CRC progression. In this review, we devote to summarize the current progress regarding the role of IL-17 in tumor initiation and progression, as well as the prognostic value in CRC. </p>","PeriodicalId":55254,"journal":{"name":"Clinical & Developmental Immunology","volume":"2013 ","pages":"436307"},"PeriodicalIF":0.0,"publicationDate":"2013-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1155/2013/436307","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"31992472","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Persistence of Th17/Tc17 cell expression upon smoking cessation in mice with cigarette smoke-induced emphysema.","authors":"Min-Chao Duan, Hai-Juan Tang, Xiao-Ning Zhong, Ying Huang","doi":"10.1155/2013/350727","DOIUrl":"10.1155/2013/350727","url":null,"abstract":"<p><p>Th17 and Tc17 cells may be involved in the pathogenesis of chronic obstructive pulmonary disease (COPD), a disease caused predominantly by cigarette smoking. Smoking cessation is the only intervention in the management of COPD. However, even after cessation, the airway inflammation may be present. In the current study, mice were exposed to room air or cigarette smoke for 24 weeks or 24 weeks followed by 12 weeks of cessation. Morphological changes were evaluated by mean linear intercepts (Lm) and destructive index (DI). The frequencies of CD8(+)IL-17(+)(Tc17) and CD4(+)IL-17(+)(Th17) cells, the mRNA levels of ROR gamma and IL-17, and the levels of IL-8, TNF-alpha, and IFN-gamma in lungs or bronchoalveolar lavage fluid of mice were assayed. Here we demonstrated that alveolar enlargement and destruction induced by cigarette smoke exposure were irreversible and that cigarette smokeenhanced these T-cell subsets, and related cytokines were not significantly reduced after smoking cessation. In addition, the frequencies of Th17 and Tc17 cells in lungs of smoke-exposed mice and cessation mice were positively correlated with emphysematous lesions. More important, the frequencies of Tc17 cells were much higher than Th17 cells, and there was a significantly positive correlation between Th17 and Tc17. These results suggested that Th17/Tc17 infiltration in lungs may play a critical role in sustaining lung inflammation in emphysema. Blocking the abnormally increased numbers of Tc17 and Th17 cells may be a reasonable therapeutic strategy for emphysema. </p>","PeriodicalId":55254,"journal":{"name":"Clinical & Developmental Immunology","volume":"2013 ","pages":"350727"},"PeriodicalIF":0.0,"publicationDate":"2013-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1155/2013/350727","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"32084460","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Baicalin inhibits IL-17-mediated joint inflammation in murine adjuvant-induced arthritis.","authors":"Xue Yang, Ji Yang, Hejian Zou","doi":"10.1155/2013/268065","DOIUrl":"https://doi.org/10.1155/2013/268065","url":null,"abstract":"<p><p>T-helper-17 (Th17) cells are implicated in a number of inflammatory disorders including rheumatoid arthritis. Antagonism of Th17 cells is a treatment option for arthritis. Here, we report that Baicalin, a compound isolated from the Chinese herb Huangqin (Scutellaria baicalensis Georgi), relieved ankle swelling and protected the joint against inflammatory destruction in a murine adjuvant-induced arthritis model. Baicalin inhibited splenic Th17 cell population expansion in vivo. Baicalin prevented interleukin- (IL-) 17-mediated lymphocyte adhesion to cultured synoviocytes. Baicalin also blocked IL-17-induced intercellular adhesion molecule 1, vascular cell adhesion molecule 1, IL-6, and tumor necrosis factor-alpha mRNA expression in cultured synoviocytes. Collectively, these findings suggest that Baicalin downregulates the joint inflammation caused by IL-17, which is likely produced by an expanded population of splenic Th17 cells in experimental arthritis. Baicalin might be a promising novel therapeutic agent for treating rheumatoid arthritis in humans. </p>","PeriodicalId":55254,"journal":{"name":"Clinical & Developmental Immunology","volume":"2013 ","pages":"268065"},"PeriodicalIF":0.0,"publicationDate":"2013-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1155/2013/268065","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"31212195","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Pivotal roles of T-helper 17-related cytokines, IL-17, IL-22, and IL-23, in inflammatory diseases.","authors":"Ning Qu, Mingli Xu, Izuru Mizoguchi, Jun-ichi Furusawa, Kotaro Kaneko, Kazunori Watanabe, Junichiro Mizuguchi, Masahiro Itoh, Yutaka Kawakami, Takayuki Yoshimoto","doi":"10.1155/2013/968549","DOIUrl":"10.1155/2013/968549","url":null,"abstract":"<p><p>T-helper 17 (Th17) cells are characterized by producing interleukin-17 (IL-17, also called IL-17A), IL-17F, IL-21, and IL-22 and potentially TNF- α and IL-6 upon certain stimulation. IL-23, which promotes Th17 cell development, as well as IL-17 and IL-22 produced by the Th17 cells plays essential roles in various inflammatory diseases, such as experimental autoimmune encephalomyelitis, rheumatoid arthritis, colitis, and Concanavalin A-induced hepatitis. In this review, we summarize the characteristics of the functional role of Th17 cells, with particular focus on the Th17 cell-related cytokines such as IL-17, IL-22, and IL-23, in mouse models and human inflammatory diseases. </p>","PeriodicalId":55254,"journal":{"name":"Clinical & Developmental Immunology","volume":"2013 ","pages":"968549"},"PeriodicalIF":0.0,"publicationDate":"2013-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1155/2013/968549","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"31666522","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Joanna Matowicka-Karna, Zbigniew Kamocki, Beata Polińska, Joanna Osada, Halina Kemona
{"title":"Platelets and inflammatory markers in patients with gastric cancer.","authors":"Joanna Matowicka-Karna, Zbigniew Kamocki, Beata Polińska, Joanna Osada, Halina Kemona","doi":"10.1155/2013/401623","DOIUrl":"10.1155/2013/401623","url":null,"abstract":"<p><p>The aim of the study was to assess the contribution of platelets and inflammatory markers in gastric cancer. We studied 50 patients. Taking into consideration the advancement of gastric cancer, patients were divided into 3 groups. Group (E)--13 patients with early gastric cancer, group (A)--18 patients with regionally advanced cancer, and group (M)--19 patients with metastatic cancer. The determinations were performed twice prior to surgery and after surgery. In patients with gastric cancer, there is an increase in IL-6 and IL-23 compared with the healthy group. The highest values of IL-6 were obtained in early cancer (more than 8-fold increase), which seems to confirm the presence of acute inflammation. The lowest value of both of these cytokines was obtained in patients with metastatic cancer. In all patients, regardless of tumor stage, there was an increase in the concentration of CRP. An increase of PLT, higher proportion of the percentage of large platelets (LPLT), and increased mean platelet volume (MPV) were observed in the process of disease development. A positive correlation between MPV and LPLT and the accompanying decrease in the concentration of proinflammatory cytokines indicates the presence of an existing relationship between the platelet morphological parameters and the inflammation process in the development of gastric cancer.</p>","PeriodicalId":55254,"journal":{"name":"Clinical & Developmental Immunology","volume":" ","pages":"401623"},"PeriodicalIF":0.0,"publicationDate":"2013-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1155/2013/401623","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"40242411","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Li Long, Ping Yu, Yanying Liu, Shiyao Wang, Ru Li, Jinxia Shi, Xiaoping Zhang, Yanmei Li, Xiaolin Sun, Bin Zhou, Liufu Cui, Zhanguo Li
{"title":"Upregulated microRNA-155 expression in peripheral blood mononuclear cells and fibroblast-like synoviocytes in rheumatoid arthritis.","authors":"Li Long, Ping Yu, Yanying Liu, Shiyao Wang, Ru Li, Jinxia Shi, Xiaoping Zhang, Yanmei Li, Xiaolin Sun, Bin Zhou, Liufu Cui, Zhanguo Li","doi":"10.1155/2013/296139","DOIUrl":"https://doi.org/10.1155/2013/296139","url":null,"abstract":"<p><strong>Objective: </strong>This study was to screen for the miRNAs differently expressed in peripheral blood mononuclear cells (PBMC) of RA, to further identify the expression of miR-155 in RA PBMC and fibroblast-like synoviocytes (FLS), and to evaluate the function of miR-155 in RA-FLS.</p><p><strong>Methods: </strong>Microarray was used to screen for differentially expressed miRNAs in RA PBMC. miR-155 expression in PBMC and FLS of RA were identified by real-time PCR. Enforced overexpression and downexpression of miR-155 were used to investigate the function of miR-155 in RA-FLS. Expression of IKBKE which was previously identified as the actual target of miR-155 was examined by Western blot and real-time PCR in RA-FLS.</p><p><strong>Results: </strong>miR-155 levels were increased in both PBMC and FLS of RA and could be induced by TNF- α . Upregulation of miR-155 decreased MMP-3 levels and suppressed proliferation and invasion of RA-FLS. Inverse relationship between the expressions of miR-155 and the MMPs production-related protein IKBKE was found.</p><p><strong>Conclusion: </strong>An inflammatory milieu may alter miRNA expression profiles in rheumatoid arthritis. miR-155 is upregulated in RA-FLS, and it may be a protective factor against the inflammatory effect in part by attenuating expression of IKBKE.</p>","PeriodicalId":55254,"journal":{"name":"Clinical & Developmental Immunology","volume":" ","pages":"296139"},"PeriodicalIF":0.0,"publicationDate":"2013-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1155/2013/296139","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"40259859","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Recent advances in the pathogenesis of autoimmune hair loss disease alopecia areata.","authors":"Taisuke Ito","doi":"10.1155/2013/348546","DOIUrl":"https://doi.org/10.1155/2013/348546","url":null,"abstract":"<p><p>Alopecia areata is considered to be a cell-mediated autoimmune disease, in which autoreactive cytotoxic T cells recognize melanocyte-associated proteins such as tyrosinase. This review discusses recent advances in the understanding of the pathogenesis of alopecia areata, focusing on immunobiology and hormonal aspects of hair follicles (HFs). The HF is a unique \"miniorgan\" with its own immune and hormonal microenvironment. The immunosuppressive milieu of the anagen hair bulb modulated by immunosuppressive factors is known as \"hair follicle immune privilege.\" The collapse of the hair follicle immune privilege leads to autoimmune reactions against hair follicle autoantigens. Alopecia areata is sometimes triggered by viral infections such as influenza that causes excess production of interferons (IFN). IFN- γ is one of the key factors that lead to the collapse of immune privilege. This paper reviews the interactions between the endocrine and immune systems and hair follicles in the pathogenesis of alopecia areata. </p>","PeriodicalId":55254,"journal":{"name":"Clinical & Developmental Immunology","volume":" ","pages":"348546"},"PeriodicalIF":0.0,"publicationDate":"2013-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1155/2013/348546","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"40259860","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Clinical characteristics of Nocardia infection in patients with rheumatic diseases.","authors":"Mieko Yamagata, Koichi Hirose, Kei Ikeda, Hiroshi Nakajima","doi":"10.1155/2013/818654","DOIUrl":"https://doi.org/10.1155/2013/818654","url":null,"abstract":"<p><p>Although Nocardiosis has considerable recurrence and mortality rates, characteristics and risk factors of Nocardia infection have not been assessed in patients with rheumatic diseases. Here, we examined the characteristics and risk factors of Nocardia infection in rheumatic disease patients in our hospital. Ten rheumatic disease patients who developed Nocardia infection were identified by retrospectively reviewing the medical records. Possible predisposing factors for Nocardia infection were high-dose glucocorticoid treatment, concomitant use of immunosuppressants, preexisting pulmonary diseases, and diabetes mellitus. All patients had pulmonary Nocardiosis, and six of them had disseminated Nocardiosis when their pulmonary lesions were identified. </p>","PeriodicalId":55254,"journal":{"name":"Clinical & Developmental Immunology","volume":" ","pages":"818654"},"PeriodicalIF":0.0,"publicationDate":"2013-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1155/2013/818654","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"40276451","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}