Cytokine signaling pathways

Tumour necrosis factor (TNF) superfamily cytokines and their receptors regulate diverse immune system functions through a common set of signalling pathways. Genetic variants in and expression of individual TNF superfamily cytokines, receptors and signalling proteins have been associated with autoimmune and inflammatory diseases, but their interconnected biology has been largely unexplored.

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After surgery, millions of people suffer from delayed healing or wound dehiscence with subsequent severe complications, even death. Previous studies have reported that ropivacaine exhibits anti-proliferative and antimigratory activities on numerous cells.

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A new study shows how a single cytokine, interleukin-4, regulates hematopoietic lineage choice by activating the JAK3–STAT6 pathway, which causes dendritic-cell-specific DNA demethylation.

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Nuclear receptor subfamily 1 group D member 1 (NR1D1), a nuclear receptor associated with a variety of physiological processes, has a low level in ovarian cancer tissues compared with adjacent normal tissues. However, its role in ovarian cancer remains unclear

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TNF is a pleiotropic cytokine and shows its biological function by binding to its receptors called TNFR1 and TNFR2. While TNFR1 induces apoptosis by activation of caspase-8 via the “death domain”, it also activates IKKα/β, MKK3/6, MKK4/7 by activation of TAK1. Although the TNFR1 signaling pathway is known by in large, it is not known how AKT and MAPKs p38, ERK1/2, and JNK1/2 are activated.

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Interleukin-27 (IL-27) is a multifunctional cytokine with both pro-inflammatory and immunoregulatory functions. At present, the role of IL-27 in pulmonary fibrosis remains unknown. This study demonstrates that IL-27 potentially attenuates BLM-induced pulmonary fibrosis by regulating Th17 differentiation and cytokine secretion.

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Rho GTPases are involved in cellular functions relevant to cancer. The roles of RhoA and Rac1 have already been established. However, the role of Rac3 in cancer aggressiveness is less well understood.

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Activation of the protein kinase B/mammalian target of rapamycin (AKT/mTOR) pathway has been demonstrated to be involved in nucleophosmin-anaplastic lymphoma kinase (NPM-ALK)-mediated tumorigenesis in anaplastic large cell lymphoma (ALCL) and correlated with unfavorable outcome in certain types of other cancers.

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Chemokine receptor signaling pathways are implicated in the pathobiology of renal cell carcinoma (RCC). However, the clinical relevance of CXCR2 receptor, mediating the effects of all angiogenic chemokines, remains unclear.

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Psoriasis is a common inflammatory skin disease characterized by abnormal keratinocyte inflammation and differentiation that has a major impact on patients’ quality of life. IL-36γ, a member of IL-36 cytokine family, is highly expressed in psoriasis and plays an important role in inflammation response and differentiation. H

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Zebrafish (Danio rerio) are an attractive vertebrate model for the molecular dissection of disease mechanisms. Janus kinase (JAK)/signal transducer and activator of transcription (stat) has been defined through studies of cytokine signaling pathways in mammals.

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IL-10 is an anti-inflammatory cytokine, participating in induction of immune tolerance and cell apoptotic death. Dendritic cells (DCs) is the most professional antigen-presenting cells among innate immune cells to exert generation and maintenance of immunological memory mediated through activation of T and B lymphocytes. The STAT signalling pathway plays a regulatory role of maturation and differentiation of immune cells.

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Stress-activated protein kinase (SAPK) signaling plays essential roles in eliciting adequate cellular responses to stresses and proinflammatory cytokines. SAPK pathways are composed of three successive protein kinase reactions. The phosphorylation of SAPK signaling components on Ser/Thr or Thr/Tyr residues suggests the involvement of various protein phosphatases in the negative regulation of these systems.

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The leptin receptor (LEPR) is a class I cytokine receptor signalling via both the janus kinase⁄signal transducer and activator of transcription (JAK⁄STAT) and the MAP kinase pathways. In addition, leptin has been shown previously to activate AMP-activated kinase (AMPK) in skeletal muscle. To enable a detailed analysis of leptin signalling in pancreatic beta cells, LEPR point mutants with single or combined exchanges of the three intracellular tyrosines were expressed in HIT-T15 insulinoma cells....

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Ligand-induced oligomerization of receptors is a key step in initiating growth factor signaling. Nevertheless, complex biological responses often require additionaltrans-signaling mechanisms involving two or more signaling cascades. For cells of neuronal origin, it was shown that neurotrophic effects evoked by nerve growth factor or other neurotro-phins dependhighlyon the cooperativitywith cytokines that belong to the transforming growth factor b (TGF-b) superfamily.

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It has been well documented that both endogenous inflammatory mediator advanced glycation end products (AGEs) and exogenous inflammatory inducer lipopolysaccharide play key roles in the initiation and development of inflammatory diseases. However, the combined inflammation-stimulatory effect of AGEs and lipopolysaccharide on endothelial cells, and, further-more, the underlying signal transduction pathways involved, have not been fully elucidated.

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Developing thymocytes and T cells express the Tec kinases Itk, Rlk⁄Txk and Tec, which are critical modulators of T-cell receptor signaling, required for full activation of phospholipase Cc, and downstream Ca 2+ and ERK-mediated signaling pathways.

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Scientifi c interest and curiosity for proteoglycan research has dramatically increased over the past decades, these molecules being no more considered as a scaffold for the cells of a given tissue, but more as a reservoir for growth factors and cytokines modulating their activation status and turnover. For example, heparin and other related heparan sulfate molecules are increasingly being recognized as important modulators of many signaling pathways.

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The ultimate goal of cancer research is the development of effective anticancer therapy. During the last several decades, the discovery of oncogenes, tumor suppressors, growth factors, signal transduction pathways has dramatically escalated our understanding of cancer cell biology and mechanisms of cell transformation.1-3 Hundreds of cellular proteins and pathways have been logically considered as molecular targets in a mechanism-based approaches of anticancer drug development.4-6 Yet, the progress in cancer treatment has not paralleled these dramatic achievements in basic research.

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The Janus kinase–signal transducer and activator of transcription (JAK–STAT) pathway is utilized by a range of cytokines (interferons, IL-2 and IL-6 amongst others) that control survival, proliferation and differentiation responses in diverse cell types. The realisation that unregulated activation of this pathway is a key driver of not only chronic inflammatory diseases such as rheumatoid arthritis, colitis and psoriasis, but also many cancers has identified its components as targets for therapeutic intervention by small molecule inhibitors and biologicals.

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