Ena-DATASET-GIS-Lilly-17-03-2016-05:23:15:322-224 - samples
Ontology highlight
ABSTRACT:
PROVIDER: EGAD00001001980 | EGA |
REPOSITORIES: EGA
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Project description:Conducted studies highlight that a mixture of genetic and environmental factors is responsible for rheumatoid arthritis (RA) development. This study aimed to analyze the available literature for the relationship between, on the one hand, single-nucleotide polymorphisms (SNPs) in the proinflammatory cytokines genes interleukin-1 (IL-1), -6, -8, -15, -17, -18, and -23, and tumor necrosis factor-alpha (TNF-α), and on the other hand, RA susceptibility, severity, and patients' response to applied treatment. The PubMed database was searched for sources. Preference was given to articles which were published within the past 20 years. Data indicate that the relationship between selected SNPs in proinflammatory cytokines genes and susceptibility to developing RA is inconclusive, and it depends on the ethnicity of the population. Although the allelic and genotypic frequencies of many SNPs in proinflammatory cytokines genes analyzed did not differ between RA patients and healthy controls, deeper analysis showed that these polymorphisms have a relationship with clinicopathological features of RA. SNPs in proinflammatory cytokines genes also "modify patients' response" to applied treatment. Further studies, on larger cohorts of subjects and in different populations, should be conducted to elucidate the role of SNPs in IL-1, -6, -8, -15, -17, -18, and -23, and TNF-α genes in RA patients.
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Project description:PURPOSE OF REVIEW:To inform readers of recent advances in our understanding of the development and function of Th17 T cells and emerging data suggesting that the interleukin-23/interleukin-17 axis may be involved in the pathogenesis of spondyloarthritis. RECENT FINDINGS:The discovery of CD4+ Th17 T cells and the interleukin-23/interleukin-17 axis has challenged existing paradigms and the role of Th1 T cells in many autoimmune diseases. The development and cytokine profile of Th17 T cells differs in mice and humans. In humans, interleukin-23 synergizes with interleukin-6 and interleukin-1 to promote Th17 development. In mice, transforming growth factor-beta and interleukin-6 are critical, whereas interleukin-23 is more important at later stages promoting interleukin-17 production. In mice, CD4+ cells producing interferon-gamma appear to be distinct from interleukin-17-producing cells, while in humans cells secreting both cytokines have been observed. Growing evidence from animal models, cytokine analyses of patient fluids, and whole-genome association studies suggest that the interleukin-23/interleukin-17 axis plays an important role in spondyloarthritis pathogenesis. Possible links between an HLA-B27-induced unfolded protein response and activation of the interleukin-23/interleukin-17 axis have been observed in animal models and may contribute to the development of the spondyloarthritis phenotype. SUMMARY:Activation of the interleukin-23/interleukin-17 axis in spondyloarthritis has important therapeutic implications.
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Project description:Psoriasis is a chronic inflammatory skin disease clinically characterized by the appearance of red colored, well-demarcated plaques with thickened skin and with silvery scales. Recent studies have established the involvement of a complex signalling network of interactions between cytokines, immune cells and skin cells called keratinocytes. Keratinocytes form the cells of the outermost layer of the skin (epidermis). Visible plaques in psoriasis are developed due to the fast proliferation and unusual differentiation of keratinocyte cells. Despite that, the exact mechanism of the appearance of these plaques in the cytokine-immune cell network is not clear. A mathematical model embodying interactions between key immune cells believed to be involved in psoriasis, keratinocytes and relevant cytokines has been developed. The complex network formed of these interactions poses several challenges. Here, we choose to study subnetworks of this complex network and initially focus on interactions involving [Formula: see text], IL-23/IL-17, and IL-15. These are chosen based on known evidence of their therapeutic efficacy. In addition, we explore the role of IL-15 in the pathogenesis of psoriasis and its potential as a future drug target for a novel treatment option. We perform steady state analyses for these subnetworks and demonstrate that the interactions between cells, driven by cytokines could cause the emergence of a psoriasis state (hyper-proliferation of keratinocytes) when levels of [Formula: see text], IL-23/IL-17 or IL-15 are increased. The model results explain and support the clinical potentiality of anti-cytokine treatments. Interestingly, our results suggest different dynamic scenarios underpin the pathogenesis of psoriasis, depending upon the dominant cytokines of subnetworks. We observed that the increase in the level of IL-23/IL-17 and IL-15 could lead to psoriasis via a bistable route, whereas an increase in the level of [Formula: see text] would lead to a monotonic and gradual disease progression. Further, we demonstrate how this insight, bistability, could be exploited to improve the current therapies and develop novel treatment strategies for psoriasis.
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