Seminars in Immunology (SEMIN IMMUNOL)

Publisher: Elsevier

Journal description

Seminars in Immunology is a review journal dedicated to keeping scientists informed of developments in the field of immunology on a topic by topic basis. Each issue is thematic in approach, devoted to an important topic of interest to immunologists, focusing on recent advances across a broad spectrum of research, from the molecular and cellular basis of the immune response to the possibilities for its manipulation. Every issue is edited by a guest editor, an internationally acknowledged expert in the field, and contains six to eight authoritative invited reviews on different aspects of the subject area. The aim of each issue is to provide a coordinated, readable, and lively review of a selected area, published rapidly to ensure currency.

Current impact factor: 5.17

Impact Factor Rankings

2015 Impact Factor Available summer 2016
2014 Impact Factor 5.17
2013 Impact Factor 6.124
2012 Impact Factor 5.926
2011 Impact Factor 6.393
2010 Impact Factor 8.337
2009 Impact Factor 9.155
2008 Impact Factor 9.114
2007 Impact Factor 7
2006 Impact Factor 10
2005 Impact Factor 8.922
2004 Impact Factor 5.734
2003 Impact Factor 5.964
2002 Impact Factor 8.705
2001 Impact Factor 6.022
2000 Impact Factor 6.544

Impact factor over time

Impact factor

Additional details

5-year impact 5.50
Cited half-life 6.70
Immediacy index 1.52
Eigenfactor 0.01
Article influence 2.45
Website Seminars in Immunology website
Other titles Seminars in immunology (Online), Seminars in immunology
ISSN 1044-5323
OCLC 36952610
Material type Document, Periodical, Internet resource
Document type Internet Resource, Computer File, Journal / Magazine / Newspaper

Publisher details


  • Pre-print
    • Author can archive a pre-print version
  • Post-print
    • Author can archive a post-print version
  • Conditions
    • Authors pre-print on any website, including arXiv and RePEC
    • Author's post-print on author's personal website immediately
    • Author's post-print on open access repository after an embargo period of between 12 months and 48 months
    • 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
    • Author's post-print may be used to update arXiv and RepEC
    • Publisher's version/PDF cannot be used
    • Must link to publisher version with DOI
    • Author's post-print must be released with a Creative Commons Attribution Non-Commercial No Derivatives License
    • Publisher last reviewed on 03/06/2015
  • Classification
    ​ green

Publications in this journal

  • Seminars in Immunology 12/2014; 26(6):429-430. DOI:10.1016/j.smim.2014.09.007
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    ABSTRACT: The CB1 cannabinoid receptor is a G protein coupled receptor that is widely expressed throughout the brain. The endogenous ligands for the CB1 receptor (endocannabinoids) are N-arachidonylethanolamine and 2-arachidonoylglycerol; together the endocannabinoids and CB1R subserve activity dependent, retrograde inhibition of neurotransmitter release in the brain. Deficiency of CB1 receptor signaling is associated with anhedonia, anxiety, and persistence of negative memories. CB1 receptor-endocannabinoid signaling is activated by stress and functions to buffer or dampen the behavioral and endocrine effects of acute stress. Its role in regulation of neuronal responses is more complex. Chronic variable stress exposure reduces endocannabinoid-CB1 receptor signaling and it is hypothesized that the resultant deficiency in endocannabinoid signaling contributes to the negative consequences of chronic stress. On the other hand, repeated exposure to the same stress can sensitize CB1 receptor signaling, resulting in dampening of the stress response. Data are reviewed that support the hypothesis that CB1 receptor signaling is stress responsive and that maintaining robust endocannabinoid/CB1 receptor signaling provides resilience against the development of stress-related pathologies.
    Seminars in Immunology 10/2014; 26(5). DOI:10.1016/j.smim.2014.04.001
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    ABSTRACT: Twenty-five years ago, immunologists and neuroscientists had little science of mutual interest. This is no longer the case. Neuroscientists now know that the first formally defined cytokine, IL-1, activates a discrete population of hypothalamic neurons. This interaction leads to the release of glucocorticoids from the adrenal gland, a hormone that has a long history in immunoregulation. Immunologists have been surprised to learn that lymphoid cells synthesize acetylcholine, the first formally recognized neurotransmitter. This neurotransmitter suppresses the synthesis of TNF. These discoveries blur the distinction of neuroscience and immunology as distinct disciplines. There are now 37 formally recognized cytokines and their receptors, and at least 60 classical neurotransmitters plus over 50 neuroactive peptides. These findings explain why both immunologists and neuroscientists are getting nervous about immunity and highlight a real need to apply integrative physiological approaches in biomedical research.
    Seminars in Immunology 10/2014; 26(5). DOI:10.1016/j.smim.2014.01.011
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    ABSTRACT: The attraction and activation of immune cells is an important response of the skin to injury and allows an efficient defense against invading pathogens. In addition, immune cells fulfill various functions that are important for the repair process. An exaggerated inflammatory response, however, is a hallmark of chronic, non-healing wounds. Therefore, it is essential to strictly control and coordinate the levels and activities of various immune cells in normal and wounded skin. Recent studies provided insight into the molecular mechanisms underlying the inflammatory response after wounding, and various transcriptional regulators involved in this process have been identified. This review summarizes our current knowledge on the function of different transcription factors in wound repair, with particular emphasis on proteins with a documented role in the control of wound inflammation.
    Seminars in Immunology 08/2014; 26(4). DOI:10.1016/j.smim.2014.01.005
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    ABSTRACT: Members of the TNFR family can play prominent roles in controlling the magnitude, duration and phenotype of the immune response to viruses. The importance of particular TNFRs in different viral infections and whether they contribute to viral control or pathology is dependent on the virus and the severity of the infection. TNFRs and their ligands are widely and differentially expressed on both adaptive and innate immune cell types. The cell types through which TNFRs exert their effects, the unique signals provided by each member of the family, and how these signals are ultimately integrated during an anti-viral immune response remain to be fully elucidated. Here we discuss the role of 4-1BB, OX40, CD27 and GITR and their ligands during viral infection and highlight some of the outstanding questions in the field.
    Seminars in Immunology 06/2014; 26(3). DOI:10.1016/j.smim.2014.05.001
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    ABSTRACT: Proteins in the TNF/TNFR superfamily are recognized as major regulators of the activity of conventional CD4 and CD8 T cells, and also of regulatory T cells (Treg). Stimulatory molecules such as OX40, CD27, GITR, DR3, CD30, 4-1BB, TACI, and TNFR2 can promote division and survival in T cells, enhance effector activity including cytokine production, and drive the generation of T cell memory. They also display the capacity to block the development of inducible Treg cells or inhibit suppressive activity in Treg cells. Additionally, molecules such as Fas, TNFR1, and TRAILR promote apoptotic death in T cells and generally limit T cell activity. Although our knowledge of these proteins is quite good at this point in time, there are still many unknowns regarding their function, their expression patterns, and the involvement of these different molecules at various stages of the T cell response that occurs in autoimmunity, cancer, infectious disease, and during vaccination. Importantly, it is still unresolved how similar or dissimilar each of these receptors are to one another, the extent to which cooperation occurs between family members, and whether alternate TNF–TNFR interactions induce qualitatively different cellular responses. All of the molecules are attractive targets for immunotherapy of human disease, but it is not yet clear how to differentiate between them and make an informed decision as to whether any one protein may be the preferred focus of clinical development for a given specific disease indication. This review will highlight unanswered questions related to these molecules and the biology of T cells, and describe possible future directions for research in this area. Expanding our knowledge of how the TNF/TNFR family control T cells will undoubtedly help fulfill the promise of these molecules for providing efficacious clinical therapy of immune system disease.
    Seminars in Immunology 06/2014; 26(3). DOI:10.1016/j.smim.2014.02.005
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    ABSTRACT: The binding of tumour necrosis factor α (TNFα) to cell surface receptors engages multiple signal transduction pathways, including three groups of mitogen-activated protein (MAP) kinases: extracellular-signal-regulated kinases (ERKs); the cJun NH2-terminal kinases (JNKs); and the p38 MAP kinases. These MAP kinase signalling pathways induce a secondary response by increasing the expression of several inflammatory cytokines (including TNFα) that contribute to the biological activity of TNFα. MAP kinases therefore function both upstream and down-stream of signalling by TNFα receptors. Here we review mechanisms that mediate these actions of MAP kinases during the response to TNFα.
    Seminars in Immunology 06/2014; 26(3). DOI:10.1016/j.smim.2014.02.009
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    ABSTRACT: TNF-like weak inducer of apoptosis (TWEAK), a TNF family ligand, and its only known signaling receptor, FGF-inducible molecule-14 (Fn14), have emerged as a key molecular pathway regulating tissue responses after acute tissue injury and in contexts of chronic injury and disease, including autoimmunity, chronic inflammation, fibrosis, and malignancy. Usually dormant due to the low level of Fn14 expression in healthy tissues, this axis is specifically activated by the upregulation of Fn14 expression locally within injured tissues, thereby triggering a wide range of activities in tissue parenchymal and stromal cells as well as tissue progenitor cells. Current evidence supports that although transient TWEAK/Fn14 pathway activation may be beneficial for tissue repair after acute injury, excessive or sustained TWEAK/Fn14 activation due to repeated injury or chronic disease mediates significant tissue damage and pathological tissue remodeling. This paradigm for the dichotomous function of the TWEAK/Fn14 pathway is discussed, highlighting emerging findings, complexities, and implications for the treatment of tissue damage-associated pathologies and cancer.
    Seminars in Immunology 06/2014; 26(3). DOI:10.1016/j.smim.2014.02.006
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    ABSTRACT: Ectodysplasin (Eda) is the most studied tumor necrosis ligand in the field of developmental biology. In all vertebrates studied so far, inactivating germline mutations in Eda lead to the genetic disease called hypohidrotic ectodermal dysplasia (HED). In humans, HED is a life-threatening condition in particular in infants due to absent or severely reduced sweating leading to hyperthermia. HED is also characterized by sparse hair, and oligo- or anodontia. Research of the Eda pathway has not only increased our knowledge on ectodermal appendage development and etiology of developmental disorders, but also on evolution of several vertebrate species including humankind. Studies on mouse and dog models of HED has led to one of the most stunning breakthroughs in applied developmental biology research by showing that a short-term treatment of neonates with a synthetic ligand corrects many of the HED-associated traits. Eighteen years after the identification of EDA as the causative gene in HED, a phase II trial aiming at permanent correction of the disease is now ongoing. This review summarizes the latest discoveries in the Eda field and points to areas that need further investigation such as the possible involvement of Eda in cell migration, stem cell maintenance, or cancer.
    Seminars in Immunology 06/2014; 26(3). DOI:10.1016/j.smim.2014.05.002
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    ABSTRACT: It has been well appreciated that the endocannabinoid system can regulate immune responses via the cannabinoid receptor 2 (CB2), which is primarily expressed by cells of the hematopoietic system. The endocannabinoid system is composed of receptors, ligands and enzymes controlling the synthesis and degradation of endocannabinoids. Along with endocannabinoids, both plant-derived and synthetic cannabinoids have been shown to bind to and signal through CB2 via G proteins leading to both inhibitory and stimulatory signals depending on the biological process. Because no cannabinoid ligand has been identified that only binds to CB2, the generation of mice deficient in CB2 has greatly expanded our knowledge of how CB2 contributes to immune cell development and function in health and disease. In regards to humans, genetic studies have associated CB2 with a variety of human diseases. Here, we review the endocannabinoid system with an emphasis on CB2 and its role in the immune system.
    Seminars in Immunology 05/2014; 26(5). DOI:10.1016/j.smim.2014.04.002
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    ABSTRACT: Human cytomegalovirus (HCMV) causes a highly prevalent and lifelong infection, with a multifaceted impact in human health. NK cells play an important role in the immune response to HCMV and the virus has reciprocally developed a variety of immune evasion strategies. We originally reported that HCMV infection promotes, to a variable degree in healthy individuals, a redistribution of the NK-cell receptor (NKR) repertoire which persists under steady-state conditions. Its hallmark is an expansion of a mature NK-cell subset displaying high surface levels of the CD94/NKG2C activating receptor, with additional distinctive phenotypic and functional features. Such adaptation of host NK cells to HCMV infection, confirmed in different clinical settings, is particularly magnified in immunocompromised patients and influenced by NKG2C gene copy number. The mechanism(s) underlying the differentiation and proliferation of NKG2C+ NK cells, the basis for the individual differences in the magnitude of their expansion, and their precise role in anti-viral defence remain open issues. Moreover, the possibility that the impact of HCMV infection on the NK-cell compartment may exert a broader influence on immunity deserves further attention.
    Seminars in Immunology 04/2014; 26(2). DOI:10.1016/j.smim.2014.03.002
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    ABSTRACT: Natural killer (NK) cells represent a first line of defense against pathogens and tumor cells. The activation of NK cells is regulated by the integration of signals deriving from activating and inhibitory receptors expressed on their surface. However, different NK cells respond differently to the same stimulus, be it target cells or agents that crosslink activating receptors. The processes that determine the level of NK cell responsiveness have been referred to collectively as NK cell education. NK cell education plays an important role in steady state conditions, where potentially auto-reactive NK cells are rendered tolerant to the surrounding environment. According to the “tuning” concept, the responsiveness of each NK cell is quantitatively adjusted to ensure self tolerance while at the same time ensuring useful reactivity against potential threats. MHC-specific inhibitory receptors displayed by NK cells play a major role in tuning NK cell responsiveness, but recent studies indicate that signaling from activating receptors is also important, suggesting that the critical determinant is an integrated signal from both types of receptors. An important and still unresolved question is whether NK cell education involves interactions with a specific cell population in the environment. Whether hematopoietic and/or non-hematopoietic cells play a role is still under debate. Recent results demonstrated that NK cell tuning exhibits plasticity in steady state conditions, meaning that it can be re-set if the MHC environment changes. Other evidence suggests, however, that inflammatory conditions accompanying infections may favor high responsiveness, indicating that inflammatory agents can over-ride the natural tendency of NK cells to adjust to the steady state environment. These findings raise many questions such as whether viruses and tumor cells manipulate NK cell responsiveness to evade immune-recognition. As knowledge of the underlying processes grows, the possibility of modulating NK cell responsiveness for therapeutic purposes is becoming increasingly attractive, and is now under serious investigation in clinical studies.
    Seminars in Immunology 04/2014; 26(2). DOI:10.1016/j.smim.2014.02.007
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    ABSTRACT: Bone marrow-derived natural killer (NK) cells constitute the major subset of cytotoxic lymphocytes in peripheral blood. They provide innate defense against intracellular infection or malignancy and contribute to immune homeostasis. Large numbers of NK cells are also present in tissues, including the liver and uterus, where they can mediate immunosurveillance but also play important roles in tissue remodeling and vascularization. Here, we review the pathways involved in NK cell lineage commitment and differentiation, discussing relationships to other lymphocyte populations and highlighting genetic determinants. Characterizing NK cells from distinct tissues and during infections have revealed subset specializations, reflecting inherent cellular plasticity. In this context, we discuss how different environmental and inflammatory stimuli may shape NK cells. Particular emphasis is placed on genes identified as being critical for NK cell development, differentiation, and function from studies of model organisms or associations with disease. Such studies are also revealing important cellular redundancies. Here, we provide a view of the genetic framework constraining NK cell development and function, pinpointing molecules required for these processes but also underscoring plasticity and redundancy that may underlie robust immunological function. With this view, built in redundancy may highlight the importance of NK cells to immunity.
    Seminars in Immunology 04/2014; 26(2). DOI:10.1016/j.smim.2014.02.003
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    ABSTRACT: Innate lymphoid cells (ILC) have recently gained much attention in immunology. They represent a novel developmentally related family. Three distinct subsets have been identified on the basis of phenotypic and functional criteria and termed ILC1, ILC2, and ILC3. The available data suggest that ILC play an important role in innate defenses against different pathogens, in lymphoid organogenesis, and in tissue remodeling. All these aspects are relevant in hematopoietic stem cell transplantation (HSCT), particularly in the haplo-HSCT setting, in which donor NK cells are known to play a major therapeutic role, while the involvement of other ILC is still undefined. In this context, it has been postulated that all ILC share a common precursor expressing the ID2 transcription factor. While the differentiation of human NK cells (belonging to ILC1) is now well characterized both in vitro and in vivo, limited information is available on the development of human ILC2 and ILC3 and of their relationships with NK cells. In this review, we will summarize the present knowledge on the developmental relationship among different ILC, with particular focus on early stages of NK cell differentiation, and their features shared with ILC2 and ILC3.
    Seminars in Immunology 04/2014; 26(2). DOI:10.1016/j.smim.2014.01.006
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    ABSTRACT: Several studies have shown that in patients with acute leukaemia given allogeneic haematopoietic stem cell transplantation (allo-HSCT) large part of the therapeutic effect lies on the anti-tumour effect displayed by cells of both adaptive and innate immunity. This evidence has also opened new scenarios for the treatment of patients with other haematological malignancies/solid tumours. In particular, donor-derived natural killer (NK) cells play a crucial role in the eradication of cancer cells in patients given an allograft from an HLA-haploidentical relative, especially when there is a killer inhibitory-receptor (KIR)–KIR ligand mismatched in the donor–recipient direction. Alloreactive donor-derived NK cells have been also demonstrated to kill recipient antigen-presenting cells and cytotoxic T lymphocytes, thus preventing graft-versus-host disease (GvHD) and graft rejection and to largely contribute to the defence against cytomegalovirus infection in the early post-transplant period. Several clinical studies have recently focused also on the influence of NK-cell activating receptors on the outcome of allo-HSCT recipients; in particular, B/x haplotype donors offer clinical advantages compared with A/A donors, even when the donor is an HLA-identical volunteer. Altogether, these data have provided the rationale for implementing phase I/II clinical trials based on adoptive infusion of either selected or ex vivo activated NK cells from an HLA-mismatched donor. This review summarizes the biological and clinical data on the role played by NK cells in patients with high-risk acute leukaemia, focusing also on the still unsolved issues and the future perspectives related to the approaches of adoptive NK cell therapy.
    Seminars in Immunology 04/2014; 26(2). DOI:10.1016/j.smim.2014.02.004
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    ABSTRACT: Natural killer (NK) cells recognize deranged cells that display stress receptors or loss of major histocompatibility complex (MHC) class I. During development, NK cells become “licensed” only after they encounter cognate human leukocyte antigen (HLA) class I, leading to the acquisition of effector function. NK cells can be exploited for cancer therapy in several ways. These include targeting with monoclonal antibodies alone or combined with ex vivo and in vivo NK cell activation to facilitate adoptive immunotherapy using donor-derived NK cell products to induce graft-vs-tumor effects. In the adoptive transfer setting, persistence and in vivo expansion requires lymphodepleting chemotherapy to prevent rejection and provide homeostatic cytokines (such as IL-15) that activate NK cells. IL-15 has the advantage of avoiding regulatory T-cell expansion. Clinical applications are currently being tested. To enhance in vivo expansion, IL-2 has been used at low doses. However, low dose administration also leads to the stimulation of regulatory T cells. Monoclonal antibodies and bispecific killer engagers (BiKEs) may enhance specificity by targeting CD16 on NK cells to tumor antigens. Inhibition of CD16 shedding may also promote enhanced cytotoxicity. Future strategies include exploiting favorable donor immunogenetics or ex vivo expansion of NK cells from blood, progenitors, or pluripotent cells. Comparative clinical trials are needed to test these approaches.
    Seminars in Immunology 04/2014; 26(2). DOI:10.1016/j.smim.2014.02.002
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    ABSTRACT: Conventional NK cells are well characterized in the mouse spleen and circulate in the blood. Less well described are NK cells found in organs such as the liver, thymus, and uterus. Recently we identified a tissue-resident NK (trNK) cell population in the liver, suggesting a potential diversity of trNK cells in other organs. In this review we compare and contrast the similarities and differences among the subpopulations of NK and innate lymphoid cells to the trNK cells in the liver.
    Seminars in Immunology 04/2014; 26(2). DOI:10.1016/j.smim.2014.01.010