Cytokine & Growth Factor Reviews RSS feed: Articles in Press. Cytokine & Growth Factor Reviews publishes thought-provoking articles (critical reviews, state-of-the-art reviews, letters to the editor, meeting reviews) devoted to important advances in the rapidly changing fields of growth factor and cytokine research. Major emphasis is placed on the multidisciplinary significance of cytokines and growth factors in areas as diverse as signal transduction, cell growth and differentiation, embryonic development, immunology, tumorigenesis and clinical medicine. http://www.cgfr.co.uk//inpress?rss=yesElsevier Inc.en © 2012 Elsevier Ltd. All rights reserved. Cytokine & Growth Factor Reviews1359-61012012-05-17 © 2012 Elsevier Ltd. All rights reserved. healthpermissions@elsevier.comhttp://www.cgfr.co.uk/article/PIIS1359610112000160/abstract?rss=yesAbstract: Interleukin (IL)-6-type cytokines are critically involved in health and disease. The duration and strength of IL-6-type cytokine-mediated signaling is tightly regulated to avoid overshooting activities. Here, molecular mechanisms of inter-familiar cytokine cross-talk are reviewed which regulate dynamics and strength of IL-6 signal transduction. Both plasticity and cytokine cross-talk are significantly involved in pro- and anti-inflammatory/regenerative properties of IL-6-type cytokines. Furthermore, we focus on IL-6-type cytokine/cytokine receptor plasticity and cross-talk exemplified by the recently identified composite cytokines IL-30/IL-6R and IL-35, the first inter-familiar IL-6/IL-12 family member. The complete understanding of the intra- and extracellular cytokine networks will aid to develop novel tailor-made therapeutic strategies with reduced side effects.Plasticity and cross-talk of Interleukin 6-type cytokines - Corrected ProofChristoph Garbers, Heike M. Hermanns, Fred Schaper, Gerhard Müller-Newen, Joachim Grötzinger, Stefan Rose-John, Jürgen Scheller10.1016/j.cytogfr.2012.04.001Cytokine & Growth Factor Reviews (2012)2012-05-17Cytokine & Growth Factor Reviews2012-05-17SURVEYhttp://www.cgfr.co.uk/article/PIIS1359610112000202/abstract?rss=yesAbstract: Inflammatory bowel disease (IBD) has unclear pathogenesis and it is related to the increasing risk of developing colorectal cancer (CRC). Recent studies have uncovered the molecular mechanism of intracellular signaling pathways of inflammatory cytokines such as tumor necrosis factor (TNF)-α, interferon (IFN)-γ and interleukin (IL)-6. The major transcription factors including STAT3 have been shown to play a major role in transmitting inflammatory cytokine signals to the nucleus. The suppressors of cytokine signaling (SOCS) 3 protein is the key physiological regulators of cytokine-mediated STAT3 signaling. As such it influences the development of inflammatory and malignant disorders like this associated with IBD. Here we review the complex function of SOCS3 in innate and adaptive immunity, different cell types (macrophages, neutrophils, dendritic cells, B cells, T cells and intestinal epithelial cells) and the role of SOCS3 on the pathogenesis of inflammatory bowel disease (IBD) and IBD-related cancer. Finally, we explore how this knowledge may open novel avenues for the rational treatment of IBD and IBD-related cancer.SOCS3 in immune regulation of inflammatory bowel disease and inflammatory bowel disease-related cancer - Corrected ProofYi Li, Colin de Haar, Maikel P. Peppelenbosch, C. Janneke van der Woude10.1016/j.cytogfr.2012.04.005Cytokine & Growth Factor Reviews (2012)2012-05-16Cytokine & Growth Factor Reviews2012-05-16SURVEYhttp://www.cgfr.co.uk/article/PIIS1359610112000196/abstract?rss=yesAbstract: Prostate cancer (PCa), the most common non-skin cancer in men, is a worldwide health concern. Treatment options for aggressive PCa are limited to androgen deprivation therapies (ADT), which are ineffective, with robust diagnostic options also being limited. The prostate specific antigen (PSA) test, for instance, is subject to high levels of false positive results and cannot distinguish between cancer confined to the prostate and aggressive metastatic cancer. As such, additional therapeutic and diagnostic options are urgently required. In recent years, a clear association between activins and prostate cancer has become evident. Activins are members of the TGF-β superfamily and are responsible for a plethora of physiological processes, including cell proliferation, apoptosis, immune surveillance, embryonic development, and follicle stimulating hormone (FSH) regulation. Activin A normally inhibits cancer development and progression, however, cancer cell growth in high-grade PCa is not inhibited by this protein. The mechanism for this apparent acquired capability to resist activin A-mediated growth inhibition is currently not well understood. Thus, the aim of this review is to analyse the role of activin A in PCa progression and to present mechanisms by which transformed cells may escape its effects. The overarching hypothesis is that insensitivity to the growth inhibitory effects of activin A is an acquired capability in PCa progression. Therefore, local and genetic elements that may be responsible for this change in cellular sensitivity to activin A during cancer progression will be highlighted with a view to identifying potential diagnostic or therapeutic targets.Insensitivity to the growth inhibitory effects of activin A: An acquired capability in prostate cancer progression - Corrected ProofEdward Ottley, Elspeth Gold10.1016/j.cytogfr.2012.04.004Cytokine & Growth Factor Reviews (2012)2012-05-14Cytokine & Growth Factor Reviews2012-05-14MINI REVIEWhttp://www.cgfr.co.uk/article/PIIS1359610112000184/abstract?rss=yesAbstract: Interleukin-6 is a classic pro-inflammatory cytokine needed to mount an effective immune response. It is secreted by a wide array of cell types, however, its target cells are more restricted, due to the fact that very few cells, except lymphocytes and hepatocytes, express the functional membrane IL-6 receptor. This therefore limits the amount of cells that can respond to IL-6. Transsignalling, the shedding of the membrane bound form of the IL-6 receptor (sIL-6R) into the local microenvironment, greatly increases the range of cells that can respond e.g. as part of a wound healing response necessary to restore the homeostatic balance. Therefore, tight regulation of IL-6 signalling must occur to stop an inappropriate wound healing response occurring. This review focusses on the role of IL-6 in inflammation and fibrosing conditions, with a particular emphasis on systemic sclerosis (SSc), a chronic autoimmune disease in which a classical hallmark of fibrosis occurs. This fibrosis, in particular the skin and internal organs, leads to contractures and internal organ failure respectively with potential fatal consequences. In this review we will discuss the biology of IL-6 in the context of fibrosing conditions such as SSc and argue why molecular targeting of IL-6 is a promising therapeutic target.Interleukin-6, its role in fibrosing conditions - Corrected ProofSteven O’Reilly, Marzena Ciechomska, Rachel Cant, Thomas Hügle, Jacob M. van Laar10.1016/j.cytogfr.2012.04.003Cytokine & Growth Factor Reviews (2012)2012-05-07Cytokine & Growth Factor Reviews2012-05-07MINI REVIEWhttp://www.cgfr.co.uk/article/PIIS1359610112000172/abstract?rss=yesAbstract: A vast number of cellular processes and signaling pathways are regulated by various receptors, ranging from transmembrane to nuclear receptors. These receptor-mediated processes are modulated by a diverse set of regulatory proteins. TNFα-induced protein 3-interacting protein 1 is such a protein that inhibits both transduction by transmembrane receptors, such as TNFα-receptor, EGF-R, and TLR, and nuclear receptors’ PPAR and RAR activity. These receptors play key roles in regulating inflammation and inflammatory diseases. A growing number of references have implicated TNIP1 through GWAS and expression studies in chronic inflammatory diseases such as psoriasis and rheumatoid arthritis, although TNIP1s exact role has yet been determined. In this review, we aim to integrate the current knowledge of TNIP1s functions with the diseases in which it has been associated to potentially elucidate the role this regulator has in promoting or alleviating these inflammatory diseases.Emerging roles for TNIP1 in regulating post-receptor signaling - Corrected ProofVincent P. Ramirez, Igor Gurevich, Brian J. Aneskievich10.1016/j.cytogfr.2012.04.002Cytokine & Growth Factor Reviews (2012)2012-04-30Cytokine & Growth Factor Reviews2012-04-30MINI REVIEW