Disease relevance of IL17B

• Radiation hybrid mapping localized the IL-17B gene to a region on human chromosome 5q that is associated with a rare autosomal recessive form of Charcot-Marie-Tooth demyelinating disease [1].
• RESULTS: RA patients expressed significantly higher levels of synovial fluid IL-20 than did the rheumatic disease controls [2].
• To investigate the relationship between IL-20 and disease activity, we examined psoriasis patients treated with the CD2-targeted agent alefacept [3].
• We also found that several types of tumor cells stained positive for IL-20, especially in squamous cell carcinoma of the skin, tongue, esophagus, and lung [4].
• Four genes--doublecortin, calpain 6, interleukin-17B, and proteolipid protein 1--were found to be overexpressed in leiomyomas compared with normal myometrium and eighteen other tissues [5].

High impact information on IL17B

• IL-17B mRNA is expressed in adult pancreas, small intestine, and stomach, whereas IL-17C mRNA is not detected by RNA blot hybridization of several adult tissues [6].
• No expression of IL-17B or IL-17C mRNA is found in activated T cells [6].
• METHODS: We analyzed IL-20 levels in synovial fluid from RA patients [2].
• Interleukin-20 (IL-20) has proinflammatory properties for keratinocytes [2].
• The effect of IL-20 on endothelial cells, neutrophils, and RASFs was investigated using MTT and migration assays [2].

Biological context of IL17B

• Expression of IL-17B in neurons and evaluation of its possible role in the chromosome 5q-linked form of Charcot-Marie-Tooth disease [1].
• Finally, to assess IL-20 function, we used microarrays to screen IL-20-treated keratinocytes, which demonstrated upregulation of disease-related and IFN-gamma-induced genes [3].

Anatomical context of IL17B

• RESULTS: During a systematic investigation of CDMPs and cytokines IL17B (chondroleukin) was found in bovine articular cartilage [7].
• DISCUSSION AND CONCLUSIONS: BMP-7 and IL17B are present in articular cartilage and synthesised in chondrocytes as shown by northern blots and real-time reverse transcription-polymerase chain reaction [7].
• In situ analysis of mouse spinal cord, dorsal root ganglia, and brain demonstrated that IL-17B mRNA is primarily expressed by the neurons [1].
• Immunohistochemical analysis of human spinal cord, dorsal root ganglia, cerebral cortex, cerebellum, and hippocampus demonstrated that IL-17B protein is primarily localized to the neuronal cell bodies and axons [1].
• Northern analysis revealed that IL-17B mRNA is expressed at very high levels in spinal cord and at much lower and more variable levels in trachea, prostate, lung, small intestine, testes, adrenal, and pancreas [1].

Physical interactions of IL17B

• GluR2 might be coupled to this synergism directly or via interleukin-17B, kinesin KIF5 or related genes also up-regulated in leiomyomata [8].

Analytical, diagnostic and therapeutic context of IL17B

• In addition, intraperitoneal injection of IL-17B purified from Chinese hamster ovary cells caused marked neutrophil migration in normal mice, in a specific and dose-dependent manner [9].
• A novel type I transmembrane protein, identified in an EST data base by homology to IL-17R, was found to bind specifically IL-17B, as determined by surface plasmon resonance analysis, flow cytometry, and co-immunoprecipitation experiments [9].
• The expression of IL-20 and its receptors in healthy rats and in rats with collagen-induced arthritis (CIA) was also analyzed [2].
• Soluble IL-20 receptor type I (sIL-20RI) or sIL-20RII was administered to rats with CIA by intramuscular electroporation, and the severity of arthritis was monitored [2].
• Tissue microarray analysis of interleukin-20 expression [4].

References