Linking genetic susceptibility to Crohnʼs disease with Th17 cell function: IL-22 serum levels are increased in Crohnʼs disease and correlate with disease activity and IL23R genotype status

Schmechel, Silke; Konrad, Astrid; Diegelmann, Julia; Glas, Jürgen; Wetzke, Martin; Paschos, Ekaterini; Lohse, Peter; Göke, Burkhard; Brand, Stephan

doi:10.1002/ibd.20315

Cited by 176 publications

(156 citation statements)

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“…Ikeuchi et al found that IL-22 promoted the proliferation of synovial fibroblasts and increased the secretion of various inflammatory mediators and cytokines, which participate in the pathogenesis of rheumatoid arthritis (27). Schmechel et al found that IL-22 serum levels in Crohn's patients were significantly higher compared to the normal controls and closely related with disease activity (19). Wolk et al found that the expression of IL-22 was unusually high in psoriatics patients (18).…”

Section: Discussionmentioning

confidence: 99%

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Diagnostic value of interleukin 22 and carcinoembryonic antigen in tuberculous and malignant pleural effusions

Jin

Chen

Wang

et al. 2011

Experimental and Therapeutic Medicine

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Abstract. The aim of this study was to investigate the diagnostic value of interleukin 22 (IL-22) and carcinoembryonic antigen (CEA) in tuberculous pleural effusions (TPEs) and malignant pleural effusions (MPEs). Pleural effusion samples from 56 patients were classified on the basis of diagnosis as TPE (n=28) and MPE (n=28). The concentration of IL-22 was determined by ELISA. Lactate dehydrogenase (LDH), adenosine dehydrogenase (ADA) and CEA levels were also determined in all patients. A significant difference was observed in the levels of ADA and CEA (P<0.01), but not in the levels of LDH (P>0.05) between TPE and MPE. The concentration of IL-22 in TPE was significantly higher compared to MPE (P<0.01). With a threshold value of 49 pg/ml, IL-22 had a sensitivity of 82.14% (23/28) and a specificity of 96.43% (27/28) for differential diagnosis. The combined detection of IL-22 and CEA had a sensitivity of 100% (28/28) and a specificity of 96.43% (27/28) to distinguish TPE from MPE. TPEs showed significantly higher levels of IL-22 compared to MPEs. The combined detection of IL-22 and CEA may be more valuable in the differential diagnosis between TPE and MPE. IntroductionPleural effusion is one of the most common clinical manifestations of pleural diseases (1-3). According to clinical risk factors and prognosis, pleural effusion can be divided into two categories, benign and malignant (4). The most common cause of benign pleural effusion is tuberculosis (TB), and that of malignant pleural effusion (MPE) is lung and breast cancer (5). Due to different risk factors and prognosis, it is necessary to differentiate between them. However, this remains a major clinical problem. Although the presence of tumor cells in pleural effusion is a diagnostic marker of MPE, the probability of finding them is low. For cytology-negative pleural effusion, some of the currently used indices, such as lactate dehydrogenase (LDH), adenosine dehydrogenase (ADA) and carcinoembryonic antigen (CEA), have a certain extent of differential value, however, their specificity and sensitivity are limited. Due to the fear of possible trauma caused by thoracoscopy, some patients are not keen to agree on such a procedure. Therefore, searching for new indices is very important.The improved understanding of pleural effusion immunopathogenesis could lead to the development of new immunodiagnostic tools to facilitate its differential diagnosis. The main cellular components in both tuberculous pleural effusions (TPEs) and MPEs are lymphocytes. Previous research data have reported that lymphocytes play an important regulatory role in the pathogenesis of pleural effusion (1,2). Inflammation leads to the accumulation of lymphocytes in the pleural cavity, which release a variety of mediators and cytokines influencing pleural capillary permeability, resulting in pleural effusion (6,7). Large scale studies have reported that CD4 + T lymphocytes play an important role in the pathogenesis of pleural effusion (7). CD4 + T cells can be differentiated into Th1, Th2, Th17...

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Section: Discussionmentioning

confidence: 99%

“…IL-22 is a member of the IL-10 family and is mainly expressed in activated T and natural killer cells. Its biological targets are epithelial or parenchymal cells in the gut, lungs, skin and kidneys (14)(15)(16) (17)(18)(19)(20). Previous studies have reported that in TPE and MPE, the levels of IL-22 are high (21,22).…”

Section: Introductionmentioning

confidence: 99%

Diagnostic value of interleukin 22 and carcinoembryonic antigen in tuberculous and malignant pleural effusions

Jin

Chen

Wang

et al. 2011

Experimental and Therapeutic Medicine

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“…It is also plausible that IL-22 may display proinflammatory and/or tissue-protective effects at different phases of the inflammatory response. With increased IL-22 levels in active lesions of IBD patients, 18,19 and increased serum levels of IL-22 correlating with disease activity in Crohn disease, 56 additional research is required to establish what factors control the outcome of IL-22 signaling in the intestine. Such information will be essential to help establish whether this cytokine can be exploited for clinical benefit.…”

Section: Th17 Cytokines In H Hepaticus Colitismentioning

confidence: 99%

Differential Requirements for IL-17A and IL-22 in Cecal versus Colonic Inflammation Induced by Helicobacter hepaticus

Morrison

Ballantyne

MacDonald

et al. 2015

The American Journal of Pathology

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Type 17 helper T-cell cytokines have been implicated in the pathogenesis of inflammatory bowel disease, a chronic condition affecting the gastrointestinal tract, but information regarding their contribution to pathology in different regions of the gut is lacking. By using a murine model of bacteria-induced typhlocolitis, we investigated the role of IL-17A, IL-17F, and IL-22 in cecal versus colonic inflammation. Cecal, but not colonic, pathology in C57BL/6 mice inoculated with Helicobacter hepaticus plus antieIL-10 receptor (IL-10R) monoclonal antibody was exacerbated by co-administration of antieIL-17A monoclonal antibody, suggesting a disease-protective role for IL-17A in the cecum. In contrast, antieIL-17F had no effect on H. hepaticus-induced intestinal pathology. Neutralization of IL-22 prevented the development of colonic, but not cecal, inflammation in H. hepaticus-infected antieIL-10Retreated mice, demonstrating a pathogenic role for IL-22 in the colon. Analysis of transcript levels revealed differential expression of IL-22R, IL-22 binding protein, and IL-23R between cecum and colon, a finding that may help explain why these tissues respond differently after antieIL-22 treatment. Analysis of microarray data from healthy human intestine further revealed significant differences in cytokine receptor transcript levels (including IL-22RA1 and IL-23R) in distinct parts of the human gut. Together, our findings demonstrate that individual type 17 helper T-cell cytokines can have proinflammatory or anti-inflammatory effects in different regions of the intestine, an observation that may have implications for interventions against human inflammatory bowel disease. (Am J Pathol 2015, 185: 3290e3303; http://dx

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“…Evidence linking T H 17 responses include elevated levels of IL-17A and IL-22 in patients suffering from inflammatory bowel disease (IBD). 105,106 A recent report also demonstrated an increased susceptibility and resistance to IBD was linked to polymorphisms in the IL-23 gene locus. 107,108 In support of this, abrogation of IL-23 in mouse models of IBD greatly attenuates disease.…”

Section: T H 17 Cells In Gut Diseasesmentioning

confidence: 99%

Manipulation of T_H17 responses in pulmonary immunity and disease through vaccination

Sonnenberg

Weiner²

2009

Human Vaccines

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Since the discovery of a novel subset of CD4 + T helper cells, T H 17 cells have been implicated in a wide range of human diseases, including autoimmunity, allergic reactions and autoinflammatory diseases. Conversely, it has also been determined that T H 17 cells are required to mount a protective immune response to a number of pathogens. It has therefore been of great interest to manipulate T H 17 responses to either prevent disease or promote immunity. Vaccination is a particularly attractive approach for this manipulation. With a focus on the pulmonary mucosal environment, we herein review T H 17 responses and potential methods for manipulation.

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Linking genetic susceptibility to Crohnʼs disease with Th17 cell function: IL-22 serum levels are increased in Crohnʼs disease and correlate with disease activity and IL23R genotype status

Cited by 176 publications

References 50 publications

Diagnostic value of interleukin 22 and carcinoembryonic antigen in tuberculous and malignant pleural effusions

Diagnostic value of interleukin 22 and carcinoembryonic antigen in tuberculous and malignant pleural effusions

Differential Requirements for IL-17A and IL-22 in Cecal versus Colonic Inflammation Induced by Helicobacter hepaticus

Manipulation of T_H17 responses in pulmonary immunity and disease through vaccination

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Linking genetic susceptibility to Crohnʼs disease with Th17 cell function: IL-22 serum levels are increased in Crohnʼs disease and correlate with disease activity and IL23R genotype status

Cited by 176 publications

References 50 publications

Diagnostic value of interleukin 22 and carcinoembryonic antigen in tuberculous and malignant pleural effusions

Diagnostic value of interleukin 22 and carcinoembryonic antigen in tuberculous and malignant pleural effusions

Differential Requirements for IL-17A and IL-22 in Cecal versus Colonic Inflammation Induced by Helicobacter hepaticus

Manipulation of TH17 responses in pulmonary immunity and disease through vaccination

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Product

Resources

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Manipulation of T_H17 responses in pulmonary immunity and disease through vaccination