Cellular Immunology (Cell Immunol )

Publisher: Elsevier

Journal description

Cellular Immunology publishes original investigations concerned with the immunological activities of cells in experimental or clinical situations. The scope of the journal encompasses the broad area of in vitro and in vivo studies of cellular immune responses. Research Areas include: Antigen receptor sites; Autoimmunity; Delayed-type hypersensitivity or cellular immunity; Immunologic deficiency states and their reconstitution Immunologic surveillance and tumor immunity; Immunomodulation; Immunotherapy; Lymphokines and cytokines; Nonantibody immunity; Parasite immunology; Resistance to intracellular microbial and viral infection; Thymus and lymphocyte immunobiology; Transplantation immunology; Tumor immunity.

Current impact factor: 1.87

Impact Factor Rankings

2015 Impact Factor Available summer 2015
2013/2014 Impact Factor 1.874
2012 Impact Factor 1.743
2011 Impact Factor 1.974
2010 Impact Factor 2.575
2009 Impact Factor 2.698
2008 Impact Factor 1.893

Impact factor over time

Impact factor

Additional details

5-year impact 2.07
Cited half-life 0.00
Immediacy index 0.28
Eigenfactor 0.01
Article influence 0.63
Website Cellular Immunology website
Other titles Cellular immunology (Online), Cellular immunology
ISSN 1090-2163
OCLC 36934751
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
    • Pre-print allowed on any website or open access repository
    • Voluntary deposit by author of authors post-print allowed on authors' personal website, arXiv.org 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

  • Source
    [Show abstract] [Hide abstract]
    ABSTRACT: Macrophages are one of the most abundant leucocytes in the intestinal mucosa where they are essential for maintaining homeostasis. However, they are also implicated in the pathogenesis of disorders such as inflammatory bowel disease (IBD), offering potential targets for novel therapies. Here we discuss the function of intestinal monocytes and macrophages during homeostasis and describe how these populations and their functions change during infection and inflammation. Furthermore, we review the current evidence that the intestinal macrophage pool requires continual renewal from circulating blood monocytes, unlike most other tissue macrophages which appear to derive from primitive precursors that subsequently self-renew.
    Cellular Immunology 09/2014;
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    ABSTRACT: Monocyte development is a tightly regulated and multi-staged process, occurring through several defined progenitor cell intermediates. The key transcription factors, including PU.1, IRF8 and KLF4, growth factors, such as M-CSF and IL-34 and cytokines that drive monocyte development from hematopoietic progenitor cells are well defined. However, the molecular controls that direct differentiation into the Ly6Chi inflammatory and Ly6Clo monocyte subsets are yet to be completely elucidated. This review will provide a summary of the transcriptional regulation of monocyte development. We will also discuss how these molecular controls are also critical for microglial development despite their distinct haematopoetic origins. Furthermore, we will examine recent breakthroughs in defining mechanisms that promote differentiation of specific monocyte subpopulations.
    Cellular Immunology 09/2014;
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    ABSTRACT: Aggregation of the high-affinity IgE receptor (FcεRI) in mast cells leads to degranulation and production of numerous cytokines and lipid mediators that promote allergic inflammation. Tyrosine phosphorylation of proteins in response to FcεRI aggregation has been implicated in mast cell activation. Here, we determined the role of PTP-PEST (encoded by PTPN12) in the regulation of mast cell activation using the RBL-2H3 rat basophilic leukemia cell line as a model. PTP-PEST expression was significantly induced upon FcεRI-crosslinking, and aggregation of FcεRI induced the phosphorylation of PTP-PEST at Ser39, thus resulting in the suppression of PTP activity. By overexpressing a phosphatase-dead mutant (PTP-PEST CS) and a constitutively active mutant (PTP-PEST SA) in RBL-2H3 cells, we showed that PTP-PEST decreased degranulation and enhanced IL-4 and IL-13 transcription in FcεRI-crosslinked RBL-2H3 cells, but PTP activity of PTP-PEST was not necessary for this regulation. However, FcεRI-induced TNF-α transcription was increased by the overexpression of PTP-PEST SA and suppressed by the overexpression of PTP-PEST CS. Taken together, these results suggest that PTP-PEST is involved in the regulation of FcεRI-mediated mast cell activation through at least two different processes represented by PTP activity-dependent and -independent pathways.
    Cellular Immunology 04/2014; 289(1-2):128-134.
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    ABSTRACT: Ischemia reperfusion injury (IRI) is critical in the pathogenesis of acute renal failure and graft rejection. Regulatory T cells (Tregs) suppress excessive immune responses in IRI. We investigated the role of CD4(+)CD25(high)CD127(low) Tregs in the early phase of renal IRI pathogenesis in a mouse model. CD4(+)CD25(high)CD127(low) Tregs in the kidney, tubular necrosis scores, and renal function were measured 24 or 72h after reperfusion. PC61, an anti-CD25 monoclonal antibody, was used to deplete Tregs before renal ischemia to confirm the effect of these Tregs. CD4(+)CD25(high)CD127(low) Tregs were expanded 24 and 72h after reperfusion. Depletion of CD4(+)CD25(high)CD127(low) Tregs was associated with worsening of renal function and histology, particularly at 72h after reperfusion. These results indicated that expansion of CD4(+)CD25(high)CD127(low) Tregs in the early phase of renal IRI may participate in tissue repair. These data reveal new insights into the pathogenesis of ischemic acute renal failure and a novel therapeutic approach.
    Cellular Immunology 04/2014; 289(1-2):106-111.
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    ABSTRACT: The vast mucosal surface of the intestine is patrolled by a large number of lymphocytes forming the intestinal immune system. Like any other system in the body, this branch of the immune system is affected by ageing. Although our knowledge on the age-associated changes of the systemic immune system has improved over the past few years, our understanding of the mechanisms of senescence of both adaptive and innate immune system of the gastrointestinal (GI) tract is still largely incomplete. However, recent advances in the field have shown that the identification of the events underlying the ageing process in the gut may have important consequences on health and wellbeing far beyond the GI-tract. The aim of this review is to summarise the impact of ageing on the intestinal immune system, including the gut epithelium and other components of the intestinal barrier that maintain intestinal immune homeostasis and shape antigen-specific immune responses.
    Cellular Immunology 04/2014; 289(1-2):112-118.
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    ABSTRACT: Clinical trials suggest that BAFF inhibitors such as atacicept (TACI-IgG) and belimumab (anti-BAFF antibody) could not reduce memory B-cell numbers, although they reduced the numbers of CD20(+) naïve B cells and activated B cells. In the present study, we explored the way to reduce memory B-cell numbers. First, we used TACI-IgG to treat murine lupus. We found that TACI-IgG was effective in reducing mature B cell numbers. Accordingly it controlled the level of the anti-dsDNA antibody in lupus-like mice. In addition, TACI-IgG up-regulated memory B cells in murine lupus. Furthermore, we found that TACI-IgG up-regulated IL-15 expression in lupus-like mice. Thus, the combination of TACI-IgG and anti-IL-15 antibodies was explored to understand their effects on the treatment of murine lupus. Compared to treatments with TACI-IgG or anti-IL-15 alone, the combination of TACI-IgG and anti-IL-15 antibodies efficiently ameliorated murine lupus phenotypes. The study provides hints for the clinical application of BAFF- and IL-15-specific therapeutic agents.
    Cellular Immunology 04/2014; 289(1-2):140-144.
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    ABSTRACT: Dendritic cells (DCs) are the major sentinel, antigen-presenting and regulatory components of the immune system. One of the central DC functions is to rapidly sense and alert host immune system of a pathogen invasion. In the present study, we investigated the role of DC exosomes (DCex) in this sentinel function. We demonstrated that DCex could bind bacterial Toll-like-receptor ligands (TLR-Ls), and acquire their ability to strongly activate bystander DCs. Consequently, bystander DCs enhance the expression of transmembrane tumor necrosis factor, secretion of proinflammatory cytokines and cross-talk with natural killer cells leading to the elevated secretion of IFNγ. These findings newly show that DCex can bind and cross-present TLR-Ls to innate-immunity effector cells, and indicate a potent mechanism to systemically alert the host immune system of pathogen invasion. They also suggest a potential novel strategy to generate effective vaccines by binding TLR-L-immune adjuvants to DCex.
    Cellular Immunology 04/2014; 289(1-2):119-127.
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    ABSTRACT: IgG-induced passive systemic anaphylaxis (PSA), a serious adverse effect of passive immune therapy using therapeutic monoclonal antibodies, has been greatly emphasized. However, controversy exists regarding the type of effector cells involved in IgG-induced anaphylaxis as a result of the induction of PSA by different IgG subtypes or the use of mice with varying genetic backgrounds. To clarify the effector cells for PSA, the PSA model with serious hypothermia was established by IgG monoclonal antibody (mAb) against natural protein or complete antigen, not hapten conjugate, in BALB/c and C57BL/6 mice. The results indicated that PSA could be remarkably inhibited by the depletion of macrophages but not by the depletion of whole leukocytes, basophils, neutrophils or monocytes. We further confirmed that macrophages are indispensable for the PSA induced by all six IgG-natural antigen complexes in both strains of mice. Additionally, platelet-activating factor (PAF) was found to be the major effector mediator for IgG-induced anaphylaxis. Moreover, gene knock-out of the third component of complement (C3) did not affect PSA-related hypothermia in C57BL/6 mice. These results indicate that macrophages and PAF act as dominant effector cells and mediator molecules, respectively, and are indispensable components in the induction of IgG-mediated PSA induced by IgG mAb and natural protein antigen. Based on the above results, we hypothesize that inconsistencies in effector cells for PSA may be associated with different features of the mAb-antigen system that might affect the magnitude of FcγRs cross-linking on effector cells.
    Cellular Immunology 04/2014; 289(1-2):97-105.
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    ABSTRACT: The INK4b-ARF-INK4a gene cluster encodes three tumor suppressors: p15(INK4b), p14(ARF), and p16(INK4a). Antisense non-coding RNA in the INK4 locus (ANRIL) is transcribed in the opposite direction from this gene cluster. Recent studies suggest that ANRIL represses the expression of p15(INK4b), p14(ARF), and p16(INK4a); however, the underlying mechanism is unclear. In this study, the expressions of ANRIL in human esophageal squamous cell carcinoma (ESCC) tissues and matched adjacent non-tumor tissues were examined by quantitative real-time polymerase chain reaction. Compared with matched adjacent non-tumor tissues, the expression levels of ANRIL in ESCC tissues were significantly increased. Furthermore, inhibition of ANRIL was found to increase the expression of p15(INK4b) and transforming growth factor β1 (TGFβ1) and depletion of ANRIL in ESCC cell lines may inhibit cellular proliferation. Thus, our findings suggest a significant role of ANRIL in the occurrence and development of ESCC through TGFβ1 signaling pathways.
    Cellular Immunology 04/2014; 289(1-2):91-96.
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    ABSTRACT: Telomeres are specific nucleoprotein structures at the end of a eukaryotic chromosomes characterized by repeats of the sequence TTAGGG and regulated by the enzyme telomerase which prevents their degradation, loss, rearrangement and end-to-end fusion. During activation, T lymphocytes actively divide, albeit through only a finite number of cell divisions due to shortening of telomeres. However, studies have demonstrated that human telomerase reverse transcriptase (hTERT), thought to be the major component regulating telomerase activity, can enhance the proliferation of T cells when overexpressed. There are many treatments for cancers, most of which are targeting the telomere and telomerase of tumor cells. However, the hTERT-transduced T cells improve their potential for proliferation, making them an appropriate cell resource for tumor adoptive immunotherapy, a procedure whereby T cells are isolated from patients, expanded ex vivo and eventually delivered back into the patients, provides a new approach for tumor therapy through improved overall survival rates in cancer patients. In this review, we will focus on the telomerase activity in T cells, the regulation of telomerase activity, and hTERT-transduced T cells used in adoptive immunotherapy for cancer.
    Cellular Immunology 04/2014; 289(1-2):63-69.
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    ABSTRACT: Transglutaminase 2 (TG2) is a ubiquitous enzyme involved in diverse biological processes. Recently, its function in adaptive immune responses has begun to emerge. Its presence and functions in B cells and T cells, for example, have been reported. However, those in dendritic cells (DCs), the principal antigen-presenting cells, are as yet unexplored in murine system. In this study, we first investigated the expression of TG2 in murine bone marrow-derived DCs, and then compared the functioning of these cells in the presence or absence of this enzyme using wild-type (WT) and TG2(-/-) mice. We found that the WT DCs expressed TG2 both in the cytoplasm and on the cell surface, both of which were elevated after LPS stimulation. Unexpectedly, between WT and TG2(-/-) DCs, there were no remarkable differences in cytokine secretion, IL-10 and IL-12, and neither in the expression of surface molecules CD80, CD86, and MHC II, excepting a moderate decrease of CD40 expression on the TG2(-/-) DCs. However, when T cells were stimulated with TG2(-/-) DCs, they showed decreased levels of proliferation, CD69 and CD25 expression, and IFN-γ secretion. The addition of anti-TG2 antibody to the WT DC-T cell co-culture resulted in decreased T cell activation. By immunofluorescence staining, TG2 was observed at DC-T cell interface (contact point). Taken together, we propose that TG2 on the surface of DCs modulates the DC-T cell interaction.
    Cellular Immunology 03/2014; 289(1-2):55-62.
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    ABSTRACT: Clinical deterioration of IgA nephropathy (IgAN) is frequently preceded by episodes of upper respiratory tract infection such as tonsillitis. The aim of this study was attempt to investigate the expression and correlation of IL-4, IFN-γ and FcαRI in tonsillar mononuclear cells under stimulations of α-hemolytic streptococcus (HS) or lipopolysaccharide (LPS) in patients with IgA nephropathy. Tonsillar mononuclear cells isolated from 26 patients with IgAN and 25 patients with chronic tonsillitis (CT) as controls were cultured for 72h with or without α-hemolytic streptococcus (HS) and lipopolysaccharide (LPS) stimulation. Concentration of IL-4 and IFN-γ level were determined by ELISA. Expression levels of IL-4, IFN-γ and FcαRI mRNA were measured by real-time PCR, respectively. FcαRI expressing cells were tracked by flow cytometry. The supernatant concentration of IL-4, IFN-γ and the expression of IL-4, IFN-γ and FcαRI mRNA in the IgA nephropathy group was markedly increased compared with the non-IgAN group. With the stimulation of HS, the production of IL-4 and the FcαRI expressing cells in the IgA nephropathy group was significantly increased than the non-IgAN group, while the secretion of IFN-γ was remarkably decreased in the IgA nephropathy group than the non-IgAN group. Upon the LPS stimulation, the concentration of IL-4, IFN-γ in the supernatant of the IgA nephropathy group was markedly increased compared with the non-IgAN group. However, there wasn't significant difference in the FcαRI expressing cells between the LPS stimulated IgAN group and the non-IgAN group. The expression of FcαRI is in a negative correlation with IL-4 while positive with IFN-γ. The tonsillar mononuclear cells of IgAN may in a state of overactive immune response, which probably can promote the secretion of Th cytokines, involving in the pathogenesis of IgAN.
    Cellular Immunology 03/2014; 289(1-2):70-75.
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    ABSTRACT: The aim of this study was to clarify the role of IL-4, IL-10, IL-13 and interferon (IFN) -γ levels in atopic asthma patients by studying the relation between their serum levels and severity of the disease. The effect of IL-10 -1082G/A and IFN-γ +874T/A SNPs was also studied. The study included 200 atopic children with asthma and 50 age- and gender matched healthy children as controls. The levels of both IL-4 and IL-13 were significantly (p<0.001) higher, while IFN-γ was significantly (p<0.001) lower in patients compared to that of the controls. There was a significant effect of gene polymorphisms of IL-10 (p<0.05) and IFN-γ (p<0.001) in occurrence of atopic asthma and increased IgE level. Polymorphism of IFN-γ gene had an effect on the serum level of IFN-γ. In conclusion, IFN-γ gene polymorphism at position +874 and IL-10 gene polymorphism at position -1082A/G are genetic determinants which contribute to susceptibility to atopic asthma in children from Saudi Arabia.
    Cellular Immunology 03/2014; 289(1-2):21-26.
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    ABSTRACT: Multiple myeloma (MM) is an incurable B-cell hematologic malignancy characterized by the clonal expansion of malignant plasma cells in the bone marrow (BM). MM cells interact with various cells within the BM microenvironment, leading to skeletal destruction, angiogenesis, and drug resistance. Therefore, control of the cell-host interaction and growth factors is important to improve patient outcome with conventional treatments. In this study, we investigated flagellin-induced cell proliferation, cytokines expression, and the mechanisms of cancer drug resistance that lead to the failure of cytotoxic therapies for MM. The human MM line KMS28BM expresses the TLR5 gene as well as the protein at high levels. When treated with the specific TLR5 ligand flagellin, KMS28BM cells showed increased proliferation, increased IgG λ production, and high-level expression and secretion of the pro-inflammatory cytokine IL-6, via NF-κB activation through p38 and PI3K/AKT signaling. Furthermore, flagellin-stimulated KMS28BM cells were shown to have "increased doxorubicin and apoptosis resistance" through the inhibition of caspases and PARP activity, and this result was reversed by blocking IL-6. Thus, increased cell viability and the chemoresistance of flagellin-stimulated KMS28BM cells may result from autocrine or paracrine signaling mediated by secreted IL-6. These findings indicate that TLR5 activation by flagellin may elicit chemoresistance in MM patients who have suffered from recurrent bacterial infections.
    Cellular Immunology 03/2014; 289(1-2):27-35.