Cytokine & growth factor reviews

Publisher: Elsevier

Journal description

Current impact factor: 6.54

Impact Factor Rankings

2015 Impact Factor Available summer 2015
2013 / 2014 Impact Factor 6.537
2012 Impact Factor 8.831
2011 Impact Factor 7.812
2010 Impact Factor 8.239
2009 Impact Factor 6.489
2008 Impact Factor 7.022
2007 Impact Factor 11.816
2006 Impact Factor 11.549
2005 Impact Factor 9.075
2004 Impact Factor 9.926
2003 Impact Factor 9.6
2002 Impact Factor 9.707
2001 Impact Factor 7.674
2000 Impact Factor 6.049

Impact factor over time

Impact factor

Additional details

5-year impact 10.79
Cited half-life 5.20
Immediacy index 0.61
Eigenfactor 0.02
Article influence 4.52
ISSN 1879-0305

Publisher details


  • Pre-print
    • Author can archive a pre-print version
  • Post-print
    • Author can archive a post-print version
  • Conditions
    • Pre-print allowed on any website or open access repository
    • Voluntary deposit by author of authors post-print allowed on authors' personal website, or institutions open scholarly website including Institutional Repository, without embargo, where there is not a policy or mandate
    • Deposit due to Funding Body, Institutional and Governmental policy or mandate only allowed where separate agreement between repository and the publisher exists.
    • Permitted deposit due to Funding Body, Institutional and Governmental policy or mandate, may be required to comply with embargo periods of 12 months to 48 months .
    • Set statement to accompany deposit
    • Published source must be acknowledged
    • Must link to journal home page or articles' DOI
    • Publisher's version/PDF cannot be used
    • Articles in some journals can be made Open Access on payment of additional charge
    • NIH Authors articles will be submitted to PubMed Central after 12 months
    • Publisher last contacted on 18/10/2013
  • Classification
    ​ green

Publications in this journal

  • [Show abstract] [Hide abstract]
    ABSTRACT: Recently it was discovered that a transient activation of transcription factor NF-κB can give cells properties essential for invasiveness and cancer initiating potential. In contrast, most oncogenes to date were characterized on the basis of mutations or by their constitutive overexpression. Study of NF-κB actually leads to a far more dynamic perspective on cancer: tumors caused by diverse oncogenes apparently evolve into cancer after loss of feedback regulation for NF-κB. This event alters the cellular phenotype and the expression of hormonal mediators, modifying signals between diverse cell types in a tissue. The result is a disruption of stem cell hierarchy in the tissue, and pervasive changes in the microenvironment and immune response to the malignant cells. Copyright © 2015 Elsevier Ltd. All rights reserved.
    Cytokine & growth factor reviews 06/2015; DOI:10.1016/j.cytogfr.2015.06.001
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    ABSTRACT: The TGF-β superfamily consists of a large group of pleiotropic cytokines that are involved in the regulation of many developmental, physiological and pathological processes. Dendritic cells are antigen-presenting cells that play a key role in innate and adaptive immune responses. Dendritic cells have a complex relationship with the TGF-β cytokine superfamily being both source and targets for many of these cytokines. Some TGF-β family members are expressed by dendritic cells and modulate immune responses, for instance through the induction of T cell polarization. Others play a crucial role in the development and function of the different dendritic cell subsets. This review summarizes the current knowledge on the role of TGF-β family cytokines in dendritic cell biology, focusing on TGF-β as well as on other, less characterized, members of these important immune mediators. Copyright © 2015 Elsevier Ltd. All rights reserved.
    Cytokine & growth factor reviews 06/2015; DOI:10.1016/j.cytogfr.2015.06.002
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    ABSTRACT: Ubiquitin is a versatile molecular signature that modulates diverse cellular processes via proteasome-dependent and proteasome-independent mechanisms. The covalent and/or non-covalent binding of mono-ubiquitin and/or poly-ubiquitin chains to a target protein broadens the dynamic and functional spectra for signal integration. Different linkages of poly-ubiquitin chains determine specific physiological or pathological functions of target proteins. Accumulating evidences has revealed the essential roles of ubiquitination in orchestrating the host defenses against cytosolic RNA or DNA from viral infections. In this review, we summarize the current progress regarding the understanding of ubiquitin-mediated regulation of the RIG-I and STING antiviral signaling pathways and discuss certain critical issues that remain to be resolved in future studies. Copyright © 2015 Elsevier Ltd. All rights reserved.
    Cytokine & growth factor reviews 04/2015; 26(3). DOI:10.1016/j.cytogfr.2015.03.001
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    ABSTRACT: Several viruses manipulate host innate immune responses to avoid immune recognition and improve viral replication and spreading. The viral protein Nef of Human Immunodeficiency Virus is mainly involved in this "hijacking" activity and is a well established virulence factor. In the last few years there have been remarkable advances in outlining a defined framework of its functions. In particular Nef appears to be a shuttling molecular adaptor able to exert its effects both on infected and non infected bystander cell. In addition it is emerging fact that it has an important impact on the chemo-cytokine network. Nef protein represents an interesting new target to develop therapeutic drugs for treatment of seropositive patients. In this review we have tried to provide a unifying view of the multiple functions of this viral protein on the basis of recently available experimental data. Copyright © 2014. Published by Elsevier Ltd.
    Cytokine & growth factor reviews 11/2014; DOI:10.1016/j.cytogfr.2014.11.010
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    ABSTRACT: Multiple Sclerosis (MS) is a progressive degenerative disorder of the central nervous system (CNS), characterized by inflammation, demyelination and axonal loss. While the majority of MS patients experience relapsing-remitting symptoms followed by a secondary progressive phase, about 10-15% patients exhibit a primary progressive disease involving continuous progression from its onset. Here we review the role of lectin-glycan recognition systems, including those concerning siglecs, C-type lectins and galectins in the pathogenesis of MS and experimental autoimmune encephalomyelitis. Particularly, we will focus on the role of galectins in the fate of T cells, dendritic cells and CNS cell populations. Understanding the regulatory circuits governed by lectin-glycan interactions and their association with disease-associated cytokine networks will contribute to develop novel therapeutic strategies in MS.
    Cytokine & growth factor reviews 06/2014; DOI:10.1016/j.cytogfr.2014.02.003
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    ABSTRACT: For about four decades, platelet-derived growth factors (PDGF) and their receptors have been the subject of intense research, revealing their roles in embryo development and human diseases. Drugs such as imatinib, which selectively inhibit the tyrosine kinase activity of these receptors, have been approved for the treatment of cancers such as gastrointestinal stromal tumors and chronic eosinophilic leukemia. Today, the interest in these factors is still increasing in relationship with new potential clinical applications in cancer, stroke, fibrosis and infectious diseases. This review focuses on the mechanisms of PDGF receptor signaling, with an emphasis on pathways that are important for disease development. Of particular interest, recent studies revealed significant differences between normal and cancer cells regarding signal transduction by these growth factors.
    Cytokine & growth factor reviews 06/2014; DOI:10.1016/j.cytogfr.2014.03.003
  • Cytokine & growth factor reviews 04/2014; 25(3). DOI:10.1016/j.cytogfr.2014.04.001
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    ABSTRACT: The TNF family ligand Ectodysplasin A (EDA) regulates the induction, morphogenesis and/or maintenance of skin-derived structures such as teeth, hair, sweat glands and several other glands. Deficiencies in the EDA - EDA receptor (EDAR) signalling pathway cause hypohidrotic ectodermal dysplasia (HED). This syndrome is characterized by the absence or malformation of several skin-derived appendages resulting in hypotrychosis, hypodontia, heat-intolerance, dry skin and dry eyes, susceptibility to airways infections and crusting of various secretions. The EDA-EDAR system is an important effector of canonical Wnt signalling in developing skin appendages. It functions by stimulating NF-κB-mediated transcription of effectors or inhibitors of the Wnt, Sonic hedgehog (SHH), Fibroblast growth factor (FGF) and Transforming growth factor beta (TGFβ) pathways that regulate interactions within or between epithelial and mesenchymal cells and tissues. In animal models of Eda-deficiency, soluble EDAR agonists can precisely correct clinically relevant symptoms with low side effects even at high agonist doses, indicating that efficient negative feedback signals occur in treated tissues. Hijacking of the placental antibody transport system can help deliver active molecules to developing foetuses in a timely manner. EDAR agonists may serve to treat certain forms of ectodermal dysplasia.
    Cytokine & growth factor reviews 04/2014; DOI:10.1016/j.cytogfr.2014.01.004
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    ABSTRACT: A breadth of studies have demonstrated the importance of GITR-GITRL in diverse immune processes. However, only a limited number of studies to date have attributed the effects of GITR/GITRL to specific cell types. Moreover, the context-dependent role of GITR/GITRL in different models makes the consequences of GITR ligation difficult to generalize. There is significant interest in the therapeutic application of GITR agonists and antagonists in human disease. Thus, the field must come to a consensus regarding the cell type-specific and physiological effects of GITR in different disease states. Here we attempt to summarize the extensive literature on GITR, to synthesize a more cohesive picture of the role of GITR/GITRL in immunity, and to identify areas that require clarification.
    Cytokine & growth factor reviews 04/2014; DOI:10.1016/j.cytogfr.2013.12.003
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    ABSTRACT: The journey from the discoveries of lymphotoxin (LT) and tumor necrosis factor (TNF) to the present day age of cytokine inhibitors as therapeutics has been an exciting one with many participants and highs and lows; the saga is compared to that in “The Wizard of Oz”. This communication summarizes the contributions of key players in the discovery of the cytokines and their receptors, the changes in nomenclature, and the discovery of the LT family’s crucial role in secondary and tertiary lymphoid organs. The remarkable advances in therapeutics are detailed as are remaining problems. Finally, special tribute is paid to two pioneers in the field who have recently passed away: Byron H. Waksman and Lloyd Old.
    Cytokine & growth factor reviews 04/2014; DOI:10.1016/j.cytogfr.2014.02.001
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    ABSTRACT: RANK and its ligand RANKL are key molecules in bone metabolism and are critically involved in pathologic bone disorders. Deregulation of the RANK/RANKL system is for example a main reason for the development of postmenopausal osteoporosis, which affects millions of women worldwide. Another essential function of RANK and RANKL is the development of a functional lactating mammary gland during pregnancy. Sex hormones, in particular progesterone, induce RANKL expression resulting in proliferation of mammary epithelial cells. Moreover, RANK and RANKL have been shown to regulate mammary epithelial stem cells. RANK and RANKL were also identified as critical mechanism in the development of hormone-induced breast cancer and metastatic spread of to bone. In this review, we will focus on the various RANK/RANKL functions ranging from bone physiology, immune regulation, and initiation of breast cancer.
    Cytokine & growth factor reviews 04/2014; DOI:10.1016/j.cytogfr.2014.01.002
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    ABSTRACT: This special issue of the Cytokine and Growth Factors Review is devoted to highlighting the exceptional science that was presented at the 14th International TNF Conference held in Québec City, Canada from July 7th - July 10th, 2013. In this beautiful and historic city, approximately 175 delegates gathered to hear and present the latest advances in the TNF superfamily (TNFSF) field across broad subjects such as cancer, signal transduction, tissue homeostasis, cell death and immunity. The science presented in oral and poster format was of the highest caliber, with exciting new stories “breaking” in this exciting inter-disciplinary area of research. We await with anticipation the next (15th) International TNF Conference to be held May 20-23rd, 2015 in Ghent, Belgium. Until then, À Bientôt!.
    Cytokine & growth factor reviews 04/2014; 25(2). DOI:10.1016/j.cytogfr.2014.03.002