European Journal of Immunology Impact Factor & Information

Publisher: European Federation of Immunological Societies, Wiley-VCH Verlag

Journal description

The European Journal of Immunology is an international journal focusing on the various aspects of immunological research. One of the world's leading journals of immunology it reports on the latest breakthroughs in the area. The European Journal of Immunology is a well-respected high-impact publication with the best Executive Committee in the field. Top authors have submitted their best papers to the journal for many years therefore building a high quality immunology journal. An ever-increasing amount of papers is being published from top authors from all over the world. The European Journal of Immunology is committed to publishing excellence with a focus on originality topicality and speed of publication. Well balanced coverage of immunology! The European Journal of Immunology provides a monthly forum for top-quality papers on the various aspects of immunological research. Original papers and short communications report the progress being made in the following fields of immunology: immunobiology experimental/human immunology molecular immunology immunopathology immunogenetics clinical immunology The Executive Committee and the international Editorial Board ensure the publication of high quality papers and an international and broad subject coverage. Kurztext Diese Zeitschrift zählt zur Weltspitze der wissenschaftlichen Immunologie-Journale. In ihr erscheinen Originalbeiträge und Kurzmitteilungen aus einem außerordentlich weiten Themengebiet. Hierzu gehören Aspekte der molekularen Immunologie der Immunogenetik der Cytokine der Immunochemie sowie der zellulären und klinischen Immunologie. Es werden außerdem Beiträge zu neuen Entwicklungen experimenteller Methoden und Techniken veröffentlicht. Society Affiliation European Federation of Immunological Societies (EFIS) Readers Immunologists biochemists molecular biologists cell biologists

Current impact factor: 4.03

Impact Factor Rankings

2015 Impact Factor Available summer 2016
2014 Impact Factor 4.034
2013 Impact Factor 4.518
2012 Impact Factor 4.97
2011 Impact Factor 5.103
2010 Impact Factor 4.942
2009 Impact Factor 5.179
2008 Impact Factor 4.865
2007 Impact Factor 4.662
2006 Impact Factor 4.772
2005 Impact Factor 4.876
2004 Impact Factor 5.005
2003 Impact Factor 4.536
2002 Impact Factor 4.832
2001 Impact Factor 4.99
2000 Impact Factor 5.24
1999 Impact Factor 5.635
1998 Impact Factor 5.438
1997 Impact Factor 5.256
1996 Impact Factor 5.701
1995 Impact Factor 6.015
1994 Impact Factor 5.664
1993 Impact Factor 5.577
1992 Impact Factor 4.934

Impact factor over time

Impact factor

Additional details

5-year impact 4.28
Cited half-life 8.50
Immediacy index 0.98
Eigenfactor 0.04
Article influence 1.69
Website European Journal of Immunology website
Other titles European journal of immunology (Online), European Journal of Immunology, EJI
ISSN 1521-4141
OCLC 41614778
Material type Document, Periodical, Internet resource
Document type Internet Resource, Computer File, Journal / Magazine / Newspaper

Publisher details

Wiley-VCH Verlag

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  • Classification

Publications in this journal

  • S Harsha Krovi · Laurent Gapin ·
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    ABSTRACT: Conventional T cells have historically been linked to exacerbating allergy. By efficiently generating primarily TH 2 cells, allergens skew the immune response to produce IL-4, IL-13, and IgE. Previously, CD1a-responsive T cells were shown to functionally respond to bee and wasp venom allergens. In this issue of the European Journal of Immunology, Subramaniam and colleagues [Eur. J. Immunol. 2015. DOI: 10.1002/eji.201545869] show that more functionally active CD1a-restricted cells are present in bee venom allergic patients than in healthy patients. Additionally, the authors show that these cells are not as frequently found in individuals receiving venom immunotherapy. Consequently, this study implicates CD1a-reactive cells as the primary responders to venom allergy, which considerably regulate the downstream immune response. This article is protected by copyright. All rights reserved.
    European Journal of Immunology 11/2015; DOI:10.1002/eji.201546157
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    ABSTRACT: Synovial fibroblast hyperplasia, T-cell hyperactivity, B-cell overactivation, and the self-perpetuating interactions among these cell types are major characteristics of rheumatoid arthritis (RA). The inflamed joints of RA patients are hypoxic, with upregulated expression of hypoxia-inducible factor-1α (HIF-1α) in RA synovial fibroblasts (RASFs). It remains unknown whether HIF-1α regulates interactions between RASFs and T cells and B cells. We report here that HIF-1α promotes the expression of inflammatory cytokines IL-6, IL-8, TNF-α and IL-1β, and cell-cell contact mediators IL-15, vascular cell adhesion molecule (VCAM)-1, thrombospondin (TSP)-1 and stromal cell-derived factor (SDF)-1 in RASFs. Furthermore, HIF-1α perpetuates RASF-mediated inflammatory Th1- and Th17-cell expansion while differentially inhibiting regulatory B10 and innate-like B cells, leading to increased IFN-γ, IL-17, and IgG production and decreased protective natural IgM secretion. Our findings suggest that HIF-1α perpetuates the interactions between RASFs and T cells and B cells to induce inflammatory cytokine and autoantibody production, thus exacerbating the severity of RA. Targeting HIF-1α may provide new therapeutic strategies for overcoming this persistent disease. This article is protected by copyright. All rights reserved.
    European Journal of Immunology 11/2015; DOI:10.1002/eji.201545784
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    ABSTRACT: Pentraxin-3 (PTX3), an acute-phase protein released during inflammation, aids phagocytic clearance of pathogens and apoptotic cells, and plays diverse immunoregulatory roles in tissue injury. Previously we showed a strong TLR2-mediated induction of PTX3 in cultured human microglia and macrophages by HspB5, which accumulates in glia during MS. Given the anti-inflammatory effects of HspB5, we examined the contribution of PTX3 to these effects in MS and its animal model EAE. Our data indicate that TLR engagement effectively induces PTX3 expression in human microglia, and that such expression is readily detectable in MS lesions. Enhanced PTX3 expression is prominently expressed in microglia in preactive MS lesions,and in microglia/macrophages engaged in myelin phagocytosis in actively demyelinating lesions. Yet, we did not detect PTX3 in cerebrospinal fluid of MS patients. PTX3 expression is also elevated in spinal cords during chronic relapsing EAE in Biozzi ABH mice, but the EAE severity and time course in PTX3-deficient mice did not differ from WT mice. Moreover, systemic PTX3 administration did not alter the disease onset or severity. Our findings reveal local functions of PTX3 during neuroinflammation in facilitating myelin phagocytosis, but do not point to a role for PTX3 in controlling the development of autoimmune neuroinflammation. This article is protected by copyright. All rights reserved.
    European Journal of Immunology 11/2015; DOI:10.1002/eji.201545950
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    ABSTRACT: Cardiomyocyte death as a result of viral infection is an excellent model for dissecting the inflammatory stress response that occurs in heart tissue. We reported earlier that a specific proteasome isoform, the immunoproteasome, prevents exacerbation of coxsackievirusB3 (CVB3) induced myocardial destruction and preserves cell vitality in heart tissue inflammation. Following the aim to decipher molecular targets of immunoproteasome-dependent proteolysis, we investigated the function and regulation of the soluble pattern recognition receptor Pentraxin3 (PTX3). We show that the ablation of PTX3 in mice aggravated CVB3-triggered inflammatory injury of heart tissue, without having any significant effect on viral titers. Thus, there might be a role of PTX3 in preventing damage-associated molecular pattern induced cell death. We found that the catalytic activity of the immunoproteasome subunit LMP7 regulates the timely availability of factors controlling PTX3 production. We report on immunoproteasome-dependent alteration of ERK1/2 and p38 mitogen-activated protein kinases, which were both found to be involved in PTX3 expression control. Our finding of a cardio-protective function of immunoproteasome-dependent PTX3 expression revealed a crucial mechanism of the stress-induced damage response in myocardial inflammation. In addition to antigen presentation and cytokine production, proteolysis by the immunoproteasome can also regulate the innate immune response during viral infection. This article is protected by copyright. All rights reserved.
    European Journal of Immunology 11/2015; DOI:10.1002/eji.201545892
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    ABSTRACT: Thymic stromal lymphopoietin (TSLP) produced by epithelial cells acts on dendritic cells (DCs) to drive differentiation of TH 2-cells, and is therefore important in allergic disease pathogenesis. However, DCs themselves make significant amounts of TSLP in response to microbial products, but little is known about the key downstream signals that induce and modulate this TSLP secretion from human DCs. We show that human monocyte-derived DC (mDC) secretion of TSLP in response to C. albicans and β-glucans requires dectin-1, Syk, NF-κB and p38 MAPK signalling. In addition, TSLP production by mDCs is greatly enhanced by IL-1β, but not TNF-α, in contrast to epithelial cells. Furthermore, TSLP secretion is significantly increased by signals emanating from the endoplasmic reticulum (ER) stress response, specifically the unfolded protein response sensors, inositol-requiring transmembrane kinase/endonuclease 1 (IRE1α) and protein kinase R-like endoplasmic reticulum kinase (PERK), which are activated by dectin-1 stimulation. Thus, TSLP production by mDCs requires the integration of signals from dectin-1, the IL-1 receptor and ER stress signalling pathways. Autocrine TSLP production is likely to play a role in mDC-controlled immune responses at sites removed from epithelial cell production of the cytokine, such as lymphoid tissue. This article is protected by copyright. All rights reserved.
    European Journal of Immunology 11/2015; DOI:10.1002/eji.201545537
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    ABSTRACT: The interaction between tissue-resident mast cells (MCs) and recruited immune cells contributes to tissue immunosurveillance. However, the cells, mechanisms and receptors involved in this cross-talk remain ill-defined. Invariant natural killer T (iNKT) cells are CD1d-restricted innate lymphocytes that recognize glycolipid antigens and have emerged as critical players in immunity. Here we show that primary mouse peritoneal MCs (PMCs) express surface CD1d, which is up-regulated in vivo following administration of alpha-galactosylceramide (αGalCer). In contrast, in bone marrow-derived MCs (BMMCs) CD1d was found to be stored intracellularly and to relocate at the cell surface upon IgE-mediated degranulation. Activated BMMCs expressing surface CD1d and loaded with αGalCer were found to induce iNKT-cell proliferation and the release of IFN-γ, IL-13 and IL-4 in a CD1d-restricted manner. Moreover, the co-stimulatory molecules CD48, CD137L, CD252, CD274 and CD275 affected MC-induced IFN-γ release and iNKT-cell proliferation. Interestingly, among the co-stimulatory molecules, CD48 and CD252 exhibited a distinctly regulatory activity on iNKT-cell release of both IFN-γ and IL-13. In conclusion, we demonstrate that the crosstalk between MCs and iNKT cells may regulate inflammatory immune responses. This article is protected by copyright. All rights reserved.
    European Journal of Immunology 11/2015; DOI:10.1002/eji.201545879
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    ABSTRACT: Tissue engineering (TE) for tissue and organ regeneration or replacement is generally performed with scaffold implants, which provide structural and molecular support to in vitro seeded or in vivo recruited cells. TE implants elicit the host immune response, often resulting in engraftment impediment or rejection. Besides this negative effect, however, the immune system components also yield a positive influence on stem cell recruitment and differentiation, allowing tissue regeneration and healing. Thus, a balanced cooperation between pro-inflammatory and pro-resolution players of the immune response is an essential element of implant success. In this context, macrophage plasticity plays a fundamental role. Therefore modulating the immune response, instead of immune suppressing the host, might be the best way to successfully implant TE tissues or organs. In particular, it is becoming evident that the scaffold, immune and stem cells are linked by a three-way interaction, and many efforts are being made for scaffold-appropriate design and functionalization in order to drive the inflammation process towards regeneration, vascularization and implant success. This review discusses current and potential strategies for inflammation modulation to aid engraftment and regeneration, supporting the concept that quality, and not quantity, of inflammation might influence implant success. This article is protected by copyright. All rights reserved.
    European Journal of Immunology 11/2015; DOI:10.1002/eji.201545818
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    ABSTRACT: The C-type lectin receptor (CTLR), Clec4d (MCL, CLECSF8), is a member of the Dectin-2 cluster of CTLRs, which also includes the related receptors Mincle and Dectin-2. Like Mincle, Clec4d recognises mycobacterial cord factor, trehalose dimycolate, and we recently demonstrated its key role in anti-mycobacterial immunity in mouse and man. Here, we characterised receptor expression in naïve mice, under inflammatory conditions, and during Mycobacterium bovis BCG infection using newly generated monoclonal antibodies. In naïve mice, Clec4d was predominantly expressed on myeloid cells within the peritoneal cavity, blood and bone marrow. Unexpectedly, basal expression of Clec4d was very low on leukocytes in the lung. However, receptor expression was significantly upregulated on pulmonary myeloid cells during Mycobacterium bovis BCG infection. Moreover, Clec4d expression could be strongly induced in vitro and in vivo by various microbial stimuli, including TLR agonists, but not exogenous cytokines. Notably, we show that Clec4d requires association with the signalling adaptor FcRγ and Mincle, but not Dectin-2, for surface expression. In addition, we provide evidence that Clec4d and Mincle, but not Dectin-2, are interdependently co-regulated during inflammation and infection. These data show that Clec4d is an inducible myeloid-expressed CTLR in mice, whose expression is tightly linked to that of Mincle. This article is protected by copyright. All rights reserved.
    European Journal of Immunology 11/2015; DOI:10.1002/eji.201545858
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    ABSTRACT: Central memory CD8(+) T cells (TCM ) play key roles in the protective immunity against infectious agents, cancer immunotherapy, and in adoptive treatments of malignant and viral diseases. CD8(+) TCM cells are characterized by specific phenotypes, homing and proliferative capacities. However, CD8(+) TCM -cell generation is challenging, and usually requires CD4(+) CD40L(+) T-cell "help" during the priming of naïve CD8(+) T cells. We have generated a replication incompetent CD40 ligand-expressing recombinant vaccinia virus (rVV40L) to promote the differentiation of human naïve CD8(+) T cells into TCM specific for viral and tumor associated antigens. Soluble CD40 ligand recombinant protein (sCD40L), and vaccinia virus wild-type (VV WT), alone or in combination, were used as controls. Here, we show that, in the absence of CD4(+) T cells, a single "in vitro" stimulation of naïve CD8(+) T cells by rVV40L-infected non-professional CD14(+) antigen presenting cells promotes the rapid generation of viral or tumor associated antigen specific CD8(+) T cells displaying TCM phenotypic and functional properties. These observations demonstrate the high ability of rVV40L to fine tune CD8(+) mediated immune responses, and strongly support the use of similar reagents for clinical immunization and adoptive immunotherapy purposes. This article is protected by copyright. All rights reserved.
    European Journal of Immunology 11/2015; DOI:10.1002/eji.201545554
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    ABSTRACT: Mesenchymal stem cells are known to exert immunomodulatory effects in inflammatory diseases. Immune-regulatory cells lead to progressive joint destruction in rheumatoid arthritis (RA). Proinflammatory cytokines, such as tumour necrosis factor α (TNF-α) and interleukins (ILs) are the main players. Here, we studied progenitor cells from RA cartilage (RA-CPCs) which are positive for IL-17 receptors to determinate the effects of inflammation on their chondrogenic potenial. IL-17A/F reduced the chondrogenic potential of these cells via the up-regulation of RUNX2 protein and enhanced IL-6 protein and MMP3 mRNA levels. Blocking antibodies against IL-17 positively influenced their repair potential. Furthermore, treating the RA-CPCs with the anti-human IL-17 antibody secukinumab or the anti-TNF-α antibody adalimumab reduced the pro-inflammatory IL-6 protein level and positively influenced the secretion of anti-inflammatory IL-10 protein. Additionally, adalimumab and secukinumab in particular reduced RUNX2 protein to promote chondrogenesis. The amelioration of inflammation, particularly via IL-17 antagonism, might be a new therapeutic approach for enhancing intrinsic cartilage repair mechanisms in RA patients. This article is protected by copyright. All rights reserved.
    European Journal of Immunology 11/2015; DOI:10.1002/eji.201545910
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    ABSTRACT: Colitis, an inflammation of the colon, is a well characterized massive tissue injury. Cytosolic phospholipase A2 α (cPLA2 α) upregulation plays an important role in the development of several inflammatory diseases. The aim of the present study was to define the role of cPLA2 α upregulation in the development of colitis. We used a mouse model of dextran sulfate sodium (DSS)-induced colitis. Immunoblotting analysis showed that cPLA2 α and NF-ĸB were upregulated and activated in the colon from day 2 of colitis induction. This molecular events preceded the development of the disease, as determined by Disease Activity Index score, body weight, colon length and the expression of colonic inflammatory markers, including neutrophil infiltration detected by myeloperoxidase and by NIMP-R14, ICAM-1, COX-2, iNOS upregulation and LTB4 and TNF-α secretion. Prevention of cPLA2 α upregulation and activity in the colon by i.v. administration of specific antisense oligonucleotides against cPLA2 α 1 day prior and every day of exposure to DSS significantly impeded the development of the disease and prevented NF-ĸB activation, neutrophils infiltration into the colonic mucosa and expression of pro-inflammatory proteins in the colon. Our results demonstrate a critical role of cPLA2 α upregulation in inflammation and development of murine colitis. This article is protected by copyright. All rights reserved.
    European Journal of Immunology 11/2015; DOI:10.1002/eji.201545848
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    ABSTRACT: Ever since its invention half a century ago, flow cytometry has been a major tool for single-cell analysis, fueling advances in our understanding of a variety of complex cellular systems, in particular the immune system. The last decade has witnessed significant technical improvements in available cytometry platforms, such that more than 20 parameters can be analyzed on a single-cell level by fluorescence-based flow cytometry. The advent of mass cytometry has pushed this limit up to, currently, 50 parameters. However, traditional analysis approaches for the resulting high-dimensional datasets, such as gating on bivariate dot plots, have proven to be inefficient. Although a variety of novel computational analysis approaches to interpret these datasets are already available, they have not yet made it into the mainstream and remain largely unknown to many immunologists. Therefore, this review aims at providing a practical overview of novel analysis techniques for high-dimensional cytometry data including SPADE, t-SNE, Wanderlust, Citrus and PhenoGraph, and how these applications can be used advantageously not only for the most complex datasets, but also for standard 14-parameter cytometry datasets. This article is protected by copyright. All rights reserved.
    European Journal of Immunology 11/2015; DOI:10.1002/eji.201545774
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    ABSTRACT: T cells expressing the γδ TCR are dominant T-cell subsets in the intestinal immune system. We previously demonstrated that γδ T cells play important roles in augmenting Th17-type colitogenic immune responses in a T-cell-induced colitic inflammation model. However, its underlying mechanism remains poorly understood. In this study, an in vitro coculture system using effector T cells enriched in gut Ag-reactive cells was employed as a readout tool to search for gut Ag presenting APCs. We found that the presence of γδ T cells dramatically enhances gut Ag presentation within the mLN in mice. Gut Ag presentation by CD11b(+) DC subsets was particularly controlled by γδ T cells. Interestingly, γδ T cell entry to the lymph nodes was essential to improve the Ag presentation. Therefore, our results highlight that γδ T cells play a previously unrecognized role to support colitogenic immunity by regulating gut Ag presentation in the draining LN. This article is protected by copyright. All rights reserved.
    European Journal of Immunology 11/2015; DOI:10.1002/eji.201545919
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    ABSTRACT: The relationship between recruitment of mononuclear phagocytes to lymphoid and gut tissues and disease in HIV and SIV infection remains unclear. To address this question, we did cross-sectional analyses of dendritic cell (DC) subsets and CD163(+) macrophages in lymph nodes (LNs) and ileum of rhesus macaques with acute and chronic SIV infection and AIDS. In LNs significant differences were only evident when comparing uninfected and AIDS groups, with loss of myeloid DCs and CD103(+) DCs from peripheral and mesenteric LNs, respectively, and accumulation of plasmacytoid DCs and macrophages in mesenteric LNs. In contrast, there were 4-fold more macrophages in ileum lamina propria in macaques with AIDS compared to chronic infection, and this increased to 40-fold in Peyer's patches. Gut macrophages exceeded plasmacytoid DCs and CD103(+) DCs by 10- to 17-fold in monkeys with AIDS but were at similar low frequencies as DCs in chronic infection. Gut macrophages in macaques with AIDS expressed IFN-α and TNF-α consistent with cell activation. CD163(+) macrophages also accumulated in gut mucosa in acute infection but lacked expression of IFN-α and TNF-α. These data reveal a relationship between inflammatory macrophage accumulation in gut mucosa and disease and suggest a role for macrophages in AIDS pathogenesis. This article is protected by copyright. All rights reserved.
    European Journal of Immunology 11/2015; DOI:10.1002/eji.201545738
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    ABSTRACT: The importance of neutrophil extracellular traps (NETs) in innate immunity is well established but the molecular mechanisms responsible for their formation are still a matter of scientific dispute. Here, we aim to characterize a possible role of the receptor-interacting protein kinase 3 (RIPK3) and the mixed lineage kinase domain-like (MLKL) signaling pathway, which are known to cause necroptosis, in NET formation. Using genetic and pharmacological approaches, we investigated whether this programmed form of necrosis is a prerequisite for NET formation. NETs have been defined as extracellular DNA scaffolds associated with the neutrophil granule protein elastase that are capable of killing bacteria. Neither Ripk3-deficient mouse neutrophils nor human neutrophils in which MLKL had been pharmacologically inactivated, exhibited abnormalities in NET formation upon physiological activation or exposure to low concentrations of PMA. These data indicate that NET formation occurs independently of both RIPK3 and MLKL signaling. This article is protected by copyright. All rights reserved.
    European Journal of Immunology 11/2015; DOI:10.1002/eji.201545615
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    ABSTRACT: In the ectopic lymphoid-like structures present in chronic inflammatory conditions such as rheumatoid arthritis (RA), a subset of human effector memory CD4(+) T cells that lacks features of follicular helper T (Tfh) cells produces CXCL13. Here we report that TGF-β induces the differentiation of human CXCL13-producing CD4(+) T cells from naïve CD4(+) T cells. The TGF-β-induced CXCL13-producing CD4(+) T cells do not express CXCR5, BCL6, and other Tfh-cell markers. Furthermore, expression levels of CD25 (IL-2Rα) in CXCL13-producing CD4(+) T cells are significantly lower than those in FoxP3(+) in vitro-induced regulatory T (iTreg) cells. Consistent with this, neutralization of IL-2 and knockdown of STAT5 clearly upregulate CXCL13 production by CD4(+) T cells, while downregulating the expression of FoxP3. Furthermore, overexpression of FoxP3 in naïve CD4(+) T cells downregulates CXCL13 production, and knockdown of FoxP3 fails to inhibit the differentiation of CXCL13-producing CD4(+) T cells. As reported in RA, proinflammatory cytokines enhance secondary CXCL13 production from reactivated CXCL13-producing CD4(+) T cells. Our findings demonstrate that CXCL13-producing CD4(+) T cells lacking Tfh-cell features differentiate via TGF-β signaling but not via FoxP3, and exert their function in IL-2-limited but TGF-β- and proinflammatory cytokine-rich inflammatory conditions. This article is protected by copyright. All rights reserved.
    European Journal of Immunology 11/2015; DOI:10.1002/eji.201546043
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    ABSTRACT: Cross-presentation is the mechanism by which exogenous antigen is processed for recognition by CD8(+) T cells. Murine CD8α(+) DCs are specialised at cross-presenting soluble and cellular antigen but in humans this process is poorly characterised. In this study we examined uptake and cross-presentation of soluble and cellular antigen by human blood CD141(+) DCs, the human equivalent of mouse CD8α(+) DCs, and compared them with human MoDCs and blood CD1c(+) DC subsets. MoDCs were superior in their capacity to internalise and cross-present soluble protein whereas CD141(+) DCs were more efficient at ingesting and cross-presenting cellular antigen. Whilst cross-presentation by CD1c(+) DCs and CD141(+) DCs was dependent on the proteasome, and hence cytosolic translocation, cross-presentation by MoDCs was not. Inhibition of endosomal acidification enhanced cross-presentation by CD1c(+) DCs and MoDCs but not by CD141(+) DCs. These data demonstrate that CD1c(+) DCs, CD141(+) DCs and MoDCs are capable of cross-presentation; however, they do so via different mechanisms. Moreover, they demonstrate that human CD141(+) DCs, like their murine CD8α(+) DC counterparts, are specialised at cross-presenting cellular antigen, most likely mediated by an enhanced capacity to ingest cellular antigen combined with subtle changes in lysosomal pH during Ag processing and use of the cytosolic pathway. This article is protected by copyright. All rights reserved.
    European Journal of Immunology 11/2015; DOI:10.1002/eji.201546023
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    ABSTRACT: This review article focuses on the rationale and evaluation of therapeutic vaccines against HIV. This strategy has been developed in order to restore or re-stimulate HIV-specific immunity in patients treated with antiretroviral therapies. Despite the lack of good candidate vaccines against HIV, two objectives have been targeted during the past 15 years. Therapeutic immunization was first proposed to help control virus relapses during treatment interruptions. More recently, the concept of therapeutic immunization has been boosted by efforts to reach HIV remission or cure, in combination to HIV reactivating agents, to help purge HIV reservoirs in a "shock and kill" strategy. This review analyses the rationales for these strategies and the results of the most widely therapeutic vaccines designed to generate T-cell immunity, i.e. recombinant viral vectors and dendritic cell-based strategies, while none of the strategies targeted HIV-specific antibodies. Only marginal control of HIV was obtained with cellular-based strategies, suggesting that approaches targeting or using broadly neutralizing antibodies, should be of benefit for future efforts of therapeutic immunization against HIV in the quest towards a cure for HIV. This article is protected by copyright. All rights reserved.
    European Journal of Immunology 11/2015; DOI:10.1002/eji.201545513