<?xml version="1.0" encoding="UTF-8"?>
<rdf:RDF xmlns:rdf="http://www.w3.org/1999/02/22-rdf-syntax-ns#" xmlns:dcterms="http://purl.org/dc/terms/" xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/" xmlns:dc="http://purl.org/dc/elements/1.1/" xmlns="http://purl.org/rss/1.0/"><channel rdf:about="http://www.cgfr.co.uk//inpress?rss=yes"><title>Cytokine &amp; Growth Factor Reviews - Articles in Press</title><description>Cytokine &amp; Growth Factor Reviews RSS feed: Articles in Press. 
 Cytokine &amp; 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.</description><link>http://www.cgfr.co.uk//inpress?rss=yes</link><dc:publisher>Elsevier Inc.</dc:publisher><dc:language>en</dc:language><dc:rights> © 2010 Elsevier Ltd. All rights reserved. </dc:rights><prism:publicationName>Cytokine &amp; Growth Factor Reviews</prism:publicationName><prism:issn>1359-6101</prism:issn><prism:publicationDate>2010-08-06</prism:publicationDate><prism:copyright> © 2010 Elsevier Ltd. All rights reserved. </prism:copyright><prism:rightsAgent>healthpermissions@elsevier.com</prism:rightsAgent><items><rdf:Seq><rdf:li rdf:resource="http://www.cgfr.co.uk/article/PIIS1359610110000493/abstract?rss=yes"/><rdf:li rdf:resource="http://www.cgfr.co.uk/article/PIIS1359610110000481/abstract?rss=yes"/><rdf:li rdf:resource="http://www.cgfr.co.uk/article/PIIS135961011000047X/abstract?rss=yes"/><rdf:li rdf:resource="http://www.cgfr.co.uk/article/PIIS1359610110000316/abstract?rss=yes"/><rdf:li rdf:resource="http://www.cgfr.co.uk/article/PIIS1359610110000365/abstract?rss=yes"/><rdf:li rdf:resource="http://www.cgfr.co.uk/article/PIIS1359610110000353/abstract?rss=yes"/><rdf:li rdf:resource="http://www.cgfr.co.uk/article/PIIS1359610110000298/abstract?rss=yes"/><rdf:li rdf:resource="http://www.cgfr.co.uk/article/PIIS1359610110000328/abstract?rss=yes"/><rdf:li rdf:resource="http://www.cgfr.co.uk/article/PIIS1359610110000286/abstract?rss=yes"/></rdf:Seq></items></channel><item rdf:about="http://www.cgfr.co.uk/article/PIIS1359610110000493/abstract?rss=yes"><title>The Yin and Yang of bone morphogenetic proteins in cancer - Corrected Proof</title><link>http://www.cgfr.co.uk/article/PIIS1359610110000493/abstract?rss=yes</link><description>Abstract: Bone morphogenetic proteins (BMPs) were first studied as growth factors or morphogens of the transforming growth factor-beta superfamily. These growth molecules, originally associated with bone and cartilage development, are now known to play an important role in morphogenesis and homeostasis in many other tissues. More recently, significant contributions from BMPs, their receptors, and interacting molecules have been linked to carcinogenesis and tumor progression. On the other hand, BMPs can sometimes function as a tumor suppressor. Our report highlights these new roles in the pathogenesis of cancer that may suggest novel targets for therapeutic intervention.</description><dc:title>The Yin and Yang of bone morphogenetic proteins in cancer - Corrected Proof</dc:title><dc:creator>Ashok Singh, Rebecca J. Morris</dc:creator><dc:identifier>10.1016/j.cytogfr.2010.06.003</dc:identifier><dc:source>Cytokine &amp; Growth Factor Reviews (2010)</dc:source><dc:date>2010-08-06</dc:date><prism:publicationName>Cytokine &amp; Growth Factor Reviews</prism:publicationName><prism:publicationDate>2010-08-06</prism:publicationDate><prism:section>SURVEY</prism:section></item><item rdf:about="http://www.cgfr.co.uk/article/PIIS1359610110000481/abstract?rss=yes"><title>NF-κB inducing kinase: A key regulator in the immune system and in cancer - Corrected Proof</title><link>http://www.cgfr.co.uk/article/PIIS1359610110000481/abstract?rss=yes</link><description>Abstract: NF-κB inducing kinase (NIK) is a kinase that activates the canonical and non-canonical NF-κB pathways to control transcriptional expression of certain proteins such as cytokines, chemokines and NF-κB signaling molecules. Many advances have been made in understanding the molecular mechanisms by which the stability of NIK is regulated to affect downstream signaling. Genetic mouse models suggest that NIK plays an essential role in the regulation of the immune system as well as in the bone microenvironment. Increasing evidence links NIK to the tumorigenesis of hematological cancers, such as multiple myeloma, and solid tumors, such as pancreatic carcinoma and melanoma. Understanding the mechanism by which NIK is de-regulated will potentially provide therapeutic options for certain diseases such as autoimmunity and cancer.</description><dc:title>NF-κB inducing kinase: A key regulator in the immune system and in cancer - Corrected Proof</dc:title><dc:creator>Yee Mon Thu, Ann Richmond</dc:creator><dc:identifier>10.1016/j.cytogfr.2010.06.002</dc:identifier><dc:source>Cytokine &amp; Growth Factor Reviews (2010)</dc:source><dc:date>2010-08-05</dc:date><prism:publicationName>Cytokine &amp; Growth Factor Reviews</prism:publicationName><prism:publicationDate>2010-08-05</prism:publicationDate></item><item rdf:about="http://www.cgfr.co.uk/article/PIIS135961011000047X/abstract?rss=yes"><title>BMP signaling in vascular development and disease - Corrected Proof</title><link>http://www.cgfr.co.uk/article/PIIS135961011000047X/abstract?rss=yes</link><description>Abstract: Genetic and functional studies indicate that common components of the bone morphogenetic protein (BMP) signaling pathway play critical roles in regulating vascular development in the embryo and in promoting vascular homeostasis and disease in the adult. However, discrepancies between in vitro and in vivo findings and distinct functional properties of the BMP signaling pathway in different vascular beds, have led to controversies in the field that have been difficult to reconcile. This review attempts to clarify some of these issues by providing an up to date overview of the biology and genetics of BMP signaling relevant to the intact vasculature.</description><dc:title>BMP signaling in vascular development and disease - Corrected Proof</dc:title><dc:creator>Jonathan W. Lowery, Mark P. de Caestecker</dc:creator><dc:identifier>10.1016/j.cytogfr.2010.06.001</dc:identifier><dc:source>Cytokine &amp; Growth Factor Reviews (2010)</dc:source><dc:date>2010-08-02</dc:date><prism:publicationName>Cytokine &amp; Growth Factor Reviews</prism:publicationName><prism:publicationDate>2010-08-02</prism:publicationDate><prism:section>SURVEY</prism:section></item><item rdf:about="http://www.cgfr.co.uk/article/PIIS1359610110000316/abstract?rss=yes"><title>IL-28A, IL-28B, and IL-29: Promising cytokines with type I interferon-like properties - Corrected Proof</title><link>http://www.cgfr.co.uk/article/PIIS1359610110000316/abstract?rss=yes</link><description>Abstract: IL-28A, IL-28B and IL-29 (also designated type III interferons) constitute a new subfamily within the IL-10–interferon family. They are produced by virtually any nucleated cell type, particularly dendritic cells, following viral infection or activation with bacterial components, and mediate their effects via the IL-28R1/IL-10R2 receptor complex. Although IL-28/IL-29 are closer to the IL-10-related cytokines in terms of gene structure, protein structure, and receptor usage, they display type I interferon-like anti-viral and cytostatic activities. Unlike type I interferons, the target cell populations of IL-28/IL-29 are restricted and mainly include epithelial cells and hepatocytes. These properties suggest that IL-28/IL-29 are potential therapeutic alternatives to type I interferons in terms of viral infections and tumors. This review describes the current knowledge about these cytokines.</description><dc:title>IL-28A, IL-28B, and IL-29: Promising cytokines with type I interferon-like properties - Corrected Proof</dc:title><dc:creator>Katrin Witte, Ellen Witte, Robert Sabat, Kerstin Wolk</dc:creator><dc:identifier>10.1016/j.cytogfr.2010.04.002</dc:identifier><dc:source>Cytokine &amp; Growth Factor Reviews (2010)</dc:source><dc:date>2010-07-26</dc:date><prism:publicationName>Cytokine &amp; Growth Factor Reviews</prism:publicationName><prism:publicationDate>2010-07-26</prism:publicationDate><prism:section>SURVEY</prism:section></item><item rdf:about="http://www.cgfr.co.uk/article/PIIS1359610110000365/abstract?rss=yes"><title>Regulation of immune cell homeostasis by type I interferons - Corrected Proof</title><link>http://www.cgfr.co.uk/article/PIIS1359610110000365/abstract?rss=yes</link><description>Abstract: Although initially identified and best characterized for their role in innate antiviral defence, type I interferons (IFN-I) are also known to have an important impact on the adaptive immune response. In part, this is linked to another long-recognised property of IFN-I, namely their ability to modify cellular proliferation and survival. Here, we review the influence of IFN-I on immune cell homeostasis, focusing on their effects on T cells and antigen-presenting cells.</description><dc:title>Regulation of immune cell homeostasis by type I interferons - Corrected Proof</dc:title><dc:creator>Fabrizio Mattei, Giovanna Schiavoni, David F. Tough</dc:creator><dc:identifier>10.1016/j.cytogfr.2010.05.002</dc:identifier><dc:source>Cytokine &amp; Growth Factor Reviews (2010)</dc:source><dc:date>2010-06-03</dc:date><prism:publicationName>Cytokine &amp; Growth Factor Reviews</prism:publicationName><prism:publicationDate>2010-06-03</prism:publicationDate><prism:section>MINI REVIEW</prism:section></item><item rdf:about="http://www.cgfr.co.uk/article/PIIS1359610110000353/abstract?rss=yes"><title>Interleukin-25: A two-edged sword in the control of immune-inflammatory responses - Corrected Proof</title><link>http://www.cgfr.co.uk/article/PIIS1359610110000353/abstract?rss=yes</link><description>Abstract: Interleukin-25 (IL-25), the newest member of the IL-17 cytokine family, initiates, promotes, and augments Th2 cell-mediated immune responses, thereby contributing to allergic disease and defense against helminthic parasites. More recent studies have shown that IL-25 can control the functional activity of non-T cells and suppress the initiation and progression of immune-mediated pathologies such as endotoxemia, colitis, experimental autoimmune encephalomyelitis, and diabetes. Taken together with the fact that IL-17 family members can form homo and heterodimers with different functions, the IL-17 family encapsulates the subtle pro and anti-inflammatory function of cytokines, which need to be understood before anti-cytokine therapy can be exploited rationally in the clinic.</description><dc:title>Interleukin-25: A two-edged sword in the control of immune-inflammatory responses - Corrected Proof</dc:title><dc:creator>Giovanni Monteleone, Francesco Pallone, Thomas T. MacDonald</dc:creator><dc:identifier>10.1016/j.cytogfr.2010.05.001</dc:identifier><dc:source>Cytokine &amp; Growth Factor Reviews (2010)</dc:source><dc:date>2010-06-02</dc:date><prism:publicationName>Cytokine &amp; Growth Factor Reviews</prism:publicationName><prism:publicationDate>2010-06-02</prism:publicationDate><prism:section>SURVEY</prism:section></item><item rdf:about="http://www.cgfr.co.uk/article/PIIS1359610110000298/abstract?rss=yes"><title>The evolution of mammalian chemokine genes - Corrected Proof</title><link>http://www.cgfr.co.uk/article/PIIS1359610110000298/abstract?rss=yes</link><description>Abstract: Chemokines play an important role in orchestrating cell recruitment and localization in both physiological and pathological conditions. More than 44 ligands have been identified in the human genome. A significantly different set of chemokines, however, is found in the mouse genome, suggesting a rapid evolution of the chemokine system in mammalian genomes. Thus, there are lineage and even individual-specific differences in chemokine genes in mammals. Differences in the expression and function between even recently duplicated genes are also evident. In this review, we discuss how evolutionary events such as gene duplication and gene conversion have shaped the diverse arrays of chemokines in mammalian genomes.</description><dc:title>The evolution of mammalian chemokine genes - Corrected Proof</dc:title><dc:creator>Hisayuki Nomiyama, Naoki Osada, Osamu Yoshie</dc:creator><dc:identifier>10.1016/j.cytogfr.2010.03.004</dc:identifier><dc:source>Cytokine &amp; Growth Factor Reviews (2010)</dc:source><dc:date>2010-05-03</dc:date><prism:publicationName>Cytokine &amp; Growth Factor Reviews</prism:publicationName><prism:publicationDate>2010-05-03</prism:publicationDate><prism:section>MINI REVIEW</prism:section></item><item rdf:about="http://www.cgfr.co.uk/article/PIIS1359610110000328/abstract?rss=yes"><title>Crosstalk between TNF and glucocorticoid receptor signaling pathways - Corrected Proof</title><link>http://www.cgfr.co.uk/article/PIIS1359610110000328/abstract?rss=yes</link><description>Abstract: TNF is a Janus-faced protein. It possesses impressive anti-tumor activities, but it is also one of the strongest known pro-inflammatory cytokines, which hampers its use as a systemic anti-cancer agent. TNF has been shown to play a detrimental role in inflammatory diseases such as rheumatoid arthritis and inflammatory bowel disease. Glucocorticoids are strongly anti-inflammatory and exert their therapeutic effects through binding to their receptor, the glucocorticoid receptor. Therefore, glucocorticoids have been used for over half a century for the treatment of inflammatory diseases. However, many patients are or become resistant to the therapeutic effects of glucocorticoids. Inflammatory cytokines have been suggested to play an important role in this steroid insensitivity or glucocorticoid resistance. This review aims to highlight the mechanisms of mutual inhibition between TNF and GR signaling pathways.</description><dc:title>Crosstalk between TNF and glucocorticoid receptor signaling pathways - Corrected Proof</dc:title><dc:creator>Tom Van Bogaert, Karolien De Bosscher, Claude Libert</dc:creator><dc:identifier>10.1016/j.cytogfr.2010.04.003</dc:identifier><dc:source>Cytokine &amp; Growth Factor Reviews (2010)</dc:source><dc:date>2010-04-26</dc:date><prism:publicationName>Cytokine &amp; Growth Factor Reviews</prism:publicationName><prism:publicationDate>2010-04-26</prism:publicationDate><prism:section>SURVEY</prism:section></item><item rdf:about="http://www.cgfr.co.uk/article/PIIS1359610110000286/abstract?rss=yes"><title>High avidity cytokine autoantibodies in health and disease: Pathogenesis and mechanisms - Corrected Proof</title><link>http://www.cgfr.co.uk/article/PIIS1359610110000286/abstract?rss=yes</link><description>Abstract: Numerous reports have documented the presence of autoantibodies working against naturally occurring cytokines in humans in health and disease. In most instances, their physiological and pathophysiological significance remains unknown. However, recent advances in the methodologies for detecting cytokine autoantibodies and their application in research focused on specific disorders have shown that some cytokine autoantibodies play an important role in the pathogenesis of disease. Additionally, levels of cytokine autoantibodies may also correlate with disease severity and progression in certain infectious and autoimmune diseases but not in others. This suggests that cytokine-specific pathogenic differences exist. While multiple lines of evidence support the notion that high avidity cytokine autoantibodies are present and likely to be ubiquitous in healthy individuals, their potential physiological role, if any, is less clear. It is believed that they may function by scavenging pro-inflammatory cytokines and thereby inhibiting deleterious ‘endocrine’ effects, or by serving as carrier proteins, providing a ‘reservoir’ of inactive cytokines and thus modulating cytokine bioactivity. A central hypothesis is that sustained or repeated high-level exposure to cytokines triggers defects in T-cell tolerance, resulting in the expansion of existing cytokine autoantibody-producing B cells.</description><dc:title>High avidity cytokine autoantibodies in health and disease: Pathogenesis and mechanisms - Corrected Proof</dc:title><dc:creator>Masato Watanabe, Kanji Uchida, Kazuhide Nakagaki, Bruce C. Trapnell, Koh Nakata</dc:creator><dc:identifier>10.1016/j.cytogfr.2010.03.003</dc:identifier><dc:source>Cytokine &amp; Growth Factor Reviews (2010)</dc:source><dc:date>2010-04-23</dc:date><prism:publicationName>Cytokine &amp; Growth Factor Reviews</prism:publicationName><prism:publicationDate>2010-04-23</prism:publicationDate><prism:section>SURVEY</prism:section></item></rdf:RDF>