Immunology Letters (IMMUNOL LETT )

Publisher: Elsevier

Description

Immunology Letters provides a vehicle for the speedy publication of full-length and short articles, Rapid Notes, (mini)Reviews and Letters to the Editor addressing all aspects of molecular and cellular immunology. The essential criteria for publication will be clarity, experimental soundness and novelty. Results contradictory to current accepted thinking or ideas divergent from actual dogmas will be considered for publication provided that they are based on solid experimental findings. Preference will be given to papers of immediate importance to other investigators, either by their experimental data, new ideas or new methodology. Scientific correspondence to the Editor-in-Chief related to the published papers may also be accepted provided that they are short and scientifically relevant to the papers mentioned, in order to provide a continuing forum for discussion. Within a reference section, new mRNA sequences with unknown function, expressed sequence tags with tissue distribution and novel monoclonal antibody descriptions are considered for publication.

  • Impact factor
    2.34
    Show impact factor history
     
    Impact factor
  • 5-year impact
    2.56
  • Cited half-life
    7.00
  • Immediacy index
    0.38
  • Eigenfactor
    0.01
  • Article influence
    0.87
  • Website
    Immunology Letters website
  • Other titles
    Immunology letters
  • ISSN
    0165-2478
  • OCLC
    5434613
  • Material type
    Periodical, Internet resource
  • Document type
    Journal / Magazine / Newspaper, Internet Resource

Publisher details

Elsevier

  • Pre-print
    • Author can archive a pre-print version
  • Post-print
    • Author can archive a post-print version
  • Conditions
    • Voluntary deposit by author of pre-print allowed on Institutions open scholarly website and pre-print servers
    • Voluntary deposit by author of authors post-print allowed on institutions open scholarly website including Institutional Repository
    • Deposit due to Funding Body, Institutional and Governmental mandate only allowed where separate agreement between repository and publisher exists
    • 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 PMC after 12 months
    • Authors who are required to deposit in subject repositories may also use Sponsorship Option
    • Pre-print can not be deposited for The Lancet
  • Classification
    ​ green

Publications in this journal

  • Immunology Letters 01/2014;
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    ABSTRACT: Highlights • An intriguing case of rituximab-induced persistent hypogammaglobulinemia was presented. • The patient also suffered from sustained lymphadenopathy and recurrent necrotizing histiocytic lymphadenopathy (Kikuchi-Fujimoto disease) accompanied by SLE-like symptoms. • Peripheral blood B cell phenotyping revealed developmental arrest to memory B cells, resemble to common variable immunodeficiency.
    Immunology Letters 10/2013;
  • Immunology Letters 10/2013;
  • Immunology Letters 01/2013;
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    ABSTRACT: The use of nanoscale materials is growing exponentially, but concerns rise about the human hazards cannot be ignored. Nanotechnology has penetrated deep into our lives in diversified areas as engineering, information technology and diagnostics. Nonetheless owing to their peculiar properties these new materials also present new health risks upon interacting with biological systems. This is a typical case of technology preceding toxicity and therefore, various toxicological aspects for an array of nanomaterials are just beginning to be assessed. Several deleterious effects are being noticed, particularly in vitro situations as well as in mammalian system. Nanoparticles toxicity is compellingly related to oxidative stress, alteration of calcium homeostasis, gene expression, pro-inflammatory responses and cellular signalling events. It is therefore critical to understand the nature and origin of the toxicity imposed by nanomaterials. Keeping all these points in mind the present review provides updated information on the various aspects such as sources of production, effect of different physical properties, interaction with biological system and mechanisms of engineered nanoparticles induced toxicities.
    Immunology Letters 01/2013;
  • Immunology Letters 01/2013;
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    ABSTRACT: Food allergy is an immune provocation induced by certain food in susceptible individuals. Most of the food allergic manifestations are evident in the individual having impaired oral tolerance. In spite of worldwide prevalence, there is no permanent cure of food allergy. Food allergic reactions are complex immunological events that comprises of several immune molecules like IgE, IL-4, IL-13 and T- cells, therefore, researchers are trying to pick the correct molecule to find out a pivotal therapeutic solutions. Being a key regulatory molecule in suppressing T-cells functional activities, cytotoxic T-cell lymphocyte antigen-4 (CTLA-4) or cluster of differentiation-152 (CD-152) has contributed a novel and revolutionary dimension towards therapeutic research of several diseases. This review focuses on different immunological and mechanistic perspectives of CTLA-4 in correlation with food allergy.
    Immunology Letters 12/2012;
  • Article: wettero
    Immunology Letters 01/2012;
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    ABSTRACT: Blood platelets express several receptors involved in immunity (e.g. complement-, toll-like- and Fcγ-receptors) and release inflammatory mediators. Furthermore, formation of platelet-leukocyte aggregates has an important role during inflammatory conditions such as coronary artery disease. Thus, apart from their well-known role in haemostasis, platelets are today also recognized as cells with immuno-modulatory properties. We have previously reported regulatory effects of complement protein 1q (C1q) on platelet activation in experimental setups using isolated cells. In the present study we have proceeded by investigating effects of C1q on collagen-induced aggregation, production of reactive oxygen species (ROS), formation of platelet-leukocyte aggregates and levels of soluble P-selectin in whole blood. Impedance measurements showed that C1q inhibited collagen-induced aggregation whereas it potentiated the collagen-provoked production of ROS in a luminol-dependent chemiluminescence assay. The effects of C1q on aggregation and ROS-production were dependent upon platelets, as they were no longer observed in presence of the platelet (GpIIb/IIIa) inhibitor Reopro. Furthermore, the levels of soluble P-selectin were found to be lowered upon treatment with C1q prior to addition of collagen. There was also a trend towards a decreased formation of large platelet-leukocyte aggregates in collagen-stimulated whole blood following C1q treatment. In conclusion, our data indicate that C1q could have a role in regulating platelet activation and associated leukocyte recruitment during vessel wall injury. This has implications for inflammatory disorders such as coronary artery disease.
    Immunology Letters 11/2011; 142(1-2):28-33.
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    ABSTRACT: Since the role of striatal GABAergic medium-sized spiny (MSP) neurons in the modulation of the immune responses is largely unknown, we evaluated the humoral immune response in rats with bilateral lesion of the striatum caused by quinolinic acid, which destroys MSP neurons. Sham-operated rats and those with striatal lesions were immunized either with TNP-LPS, a T-independent antigen type 1, or one of several T-dependent antigens: ovoalbumin, bovine serum albumin, lysozyme, sheep red blood cells (SRBC) or outer membrane proteins (OMP) of Salmonella enterica serovar Typhimurium. The specific levels of serum IgM and IgG, as well as intestinal IgA antibodies were determined either by enzyme-linked immunosorbent assay (ELISA) or a haemagglutination assay 5 or 7 days after immunization. Our results show that the lesion of striatal MSP neurons attenuated the primary antibody response to the T-independent antigen type 1 (TNP-LPS), but increased the antibody response to T-dependent antigens (proteins, SRBC and OMP), indicating that the striatal neurons modulate the humoral immune response in rats. The mechanisms involved are probably related to a reduction in both the number of B cells and the expression of caveolin-1 in the spleen, as well as an increase in the number of CD4(+) T cells and in corticosterone levels of the serum.
    Immunology Letters 10/2008; 120(1-2):20-8.
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    ABSTRACT: Pemphigus is a severe blistering disease of the skin and mucous membranes caused by pathogenic autoantibodies to desmosomal adhesion proteins desmoglein-3 (Dsg3) and desmoglein-1 (Dsg1). The antibody titer and the distinct isotype patterns correlated with the disease activity. To identify their functional properties and pathogenic potential, we immunized C57BL/6 and Balb/c mice with recombinant Dsg3 fusion protein plus complete Freund's adjuvant (CFA) or Aluminum Hydroxide hydrate (Alum). After immunization, the cytokine profiles on T cells, the antibody titers, and the isotypes were analyzed. The pathogenicity of different autoantibody isotypes was evaluated by antibody passive transfer approach. It was found that Th1 type cytokine interferon gamma (IFN gamma) was elevated in the CFA-treated group, while Th2 type cytokine interleukin-4 (IL-4) was increased in the Alum-treated group. IgG1 expression was persistent in the Alum group while IgG2a was predominant in the CFA group. Neonatal mice transferred with sera from the Alum group, but not the CFA group, developed skin lesions clinically and histologically with IgG deposition on the epidermal keratinocytes. Our findings suggest that distinct T cell responses could be switched after active immunization combined with different adjuvants, resulting in distinct anti-Dsg3 antibody isotypes with different pathogenic activities in disease development. These findings shed new light on the immunopathogenesis of PV and offer a new therapeutic strategy for this potentially fatal disorder.
    Immunology Letters 10/2008; 120(1-2):6-13.
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    ABSTRACT: Dendritic cells (DC) mediate potent alloimmune responses through the positive costimulatory molecules CD40, CD80 and CD86 while the negative costimulatory molecules, immunoglobulin-like transcript 2 (ILT2), ILT3 and ILT4 have been associated with tolerogenic DC function. Due to the pivotal role played by DC in immunity the effect of the immunosuppressive agent rapamycin (RAPA) on the expression profile of both positive and negative costimulatory molecules during human DC differentiation and maturation was investigated. During monocyte differentiation to DC an increase in the mean fluorescence intensity (MFI) for CD40, CD80, CD83 and CD86 was observed in association with a concomitant downregulation of ILT2, ILT3, ILT4 and HLA-G expression. While DC differentiation in the presence of RAPA (10nM) showed a reduction in the MFI for CD40, CD80 and CD86 expressing cells, treatment after differentiation had no effect on the expression of these costimulatory molecules. The inhibitory receptors were also downregulated by RAPA only when added during differentiation. In comparison to RAPA, Cyclosporin A (CsA) had relatively minor effects on DC phenotype whereas IFN-alpha showed induction of CD80, CD86 and HLA-G when added prior to differentiation. Functionally, RAPA-treated DC used as stimulators in a DC-T cell mixed lymphocyte reaction (MLR) showed 40% inhibition of T cell proliferation relative to untreated DC (P=0.001) whereas CsA-treated DC showed no difference, and IFN-alpha-treated DC stimulated T cell proliferation. Nevertheless, the induction of T cell hyporesponsiveness by coculture of RAPA-treated DC with T cells was not associated with the generation of increased numbers of FoxP3 positive T regulatory cells. In conclusion, although RAPA downregulated ILT2, ILT3 and ILT4 expression in DC, the inhibition of T cell proliferation by RAPA-treated DC is predominantly due to the reduction of CD40, CD80 and CD86 expression rather than the propensity to generate FoxP3 expressing regulatory cells.
    Immunology Letters 10/2008; 120(1-2):49-56.
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    ABSTRACT: Although cytotoxic T lymphocyte-associated antigen-4 (CTLA-4) inhibits T cell activation when ligated by B7 molecules on antigen-presenting cells, it can also act as an activating receptor when binding certain soluble recombinant ligands known as inverse agonists. Following ligation with an inverse agonist, we observed CTLA-4 microclusters evenly distributed on the T cell surface over a 60-min period. We have previously shown that the inverse agonist properties of these ligands correlate with their capacity to induce the formation of large CTLA-4 oligomers that are distinctly different from those resulting by CTLA-4 engagement with membrane-bound B7. These oligomers are composed of CTLA-4 molecules expressed on the cell surface and decrease from both the soluble cell lysate and lipid rafts upon cellular fractionation. Formation of these inverse agonist-induced CTLA-4 oligomers does not require an intact actin cytoskeleton. However, modulation of these oligomers was partially blocked upon actin depolymerization. Retention of CTLA-4 oligomers on the cell surface correlated with enhanced T cell signaling. Together, our data further characterize the structural basis of inverse agonist properties for CTLA-4 ligands that may be used in the design and screening of therapeutic biologicals targeting this receptor.
    Immunology Letters 10/2008; 120(1-2):29-36.
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    ABSTRACT: Inflammation is an important event in the development of vascular diseases such as hypertension, atherosclerosis, and restenosis. In addition, the stimulation of Toll-like receptor 4 (TLR4) by lipopolysaccharide (LPS) induces the release of critical proinflammatory cytokines that activate potent immune responses. In this study, LPS was found to induce TLR4 expression and increased nitric oxide (NO) production by increasing the expression of inducible nitric oxide synthase (iNOS). Furthermore, LPS was found to induce interleukin (IL)-8 and vascular endothelial growth factor (VEGF) production, as well as intracellular adhesion molecule-1 (ICAM-1) and vascular cell adhesion molecule-1 (VCAM-1) expression. Taken together, these results indicate that LPS induces inflammatory responses in HASMC. Moreover, NOS inhibitor (L-NAME) and anti-TLR 4mAb reduced the LPS-induced NO, IL-8 and VEGF production and ICAM-1 expression. Additionally, TLR4 expression was reduced by NOS inhibitor. Taken together, these results indicate that LPS-induced inflammatory responses are regulated by TLR4 expression and NO production.
    Immunology Letters 10/2008; 120(1-2):57-64.
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    ABSTRACT: Previously, we found that more than a half of the NK1.1(+) T cell lines prepared from CD1(-/-) livers expressed invariant Valpha19-Jalpha33 TCR alpha chains. Over-expression of the invariant Valpha19-Jalpha33 TCR alpha transgene (Tg) with a natural TCR alpha promoter and an enhancer in mice induced the development of NK1.1(+) T cells (Valpha19 NKT cells) in the lymphoid organs, especially in the liver. Preferential usage of the Valpha19 Tg by NKT cells in the transgenic mouse livers was indirectly indicated by the observation that few NK1.1(+) TCRalphabeta(+) cells of the Valpha19 Tg livers were stained with a cocktail of anti-TCR Valpha antibodies in the FACS analysis. Upon invariant TCR engagement in vivo following injection of mice with anti-CD3 antibody, NKT cells of the Tg mouse livers as well as spleens promptly produced immunoregulatory cytokines such as IL-4 and IFN-gamma and altered surface receptor expression. Collectively, localization of Valpha19 NKT cells in the liver is suggested that are ready to immediately response against antigen stimulation.
    Immunology Letters 10/2008; 121(1):38-44.
  • Immunology Letters 10/2008; 121(1):84-5.
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    ABSTRACT: Functional impairment of dendritic cells (DC) appears to be one of the mechanisms responsible for tumor escape from the control of the immune system. DC isolated from tumor-bearing animals and cancer patients with solid or with hematological malignancies have phenotypic and functional abnormalities. In addition, supernatants from in vitro cultured tumor cells have been shown to interfere with DC differentiation from CD34+ and monocyte precursors. Primary effusion lymphoma (PEL) is a Human Herpesvirus-8 (HHV-8)-associated tumor, which releases several cytokines such as IL-6, IL-10 and VEGF and its growth seems to be dependent on them in vitro or in vivo. In the present study, we found that these cytokines released by PELs have also an important role in interfering with the in vitro differentiation of immature DC (iDC) from CD14+ monocytes. The iDC obtained in the presence of PEL supernatants showed reduction of FITC-dextran uptake, reduction of MLR allostimulatory activity and altered expression of surface molecules, suggesting that cytokines released by PEL adversely affect DC differentiation.
    Immunology Letters 10/2008; 120(1-2):37-41.
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    ABSTRACT: Activation of resting T cells is highly dependent on dendritic cells (DCs), which take up antigens and present antigenic peptides to T cells in the context of the major histocompatibility complex (MHC). In this study, we generated a monoclonal antibody, which we call 1C4 that recognizes integrin alpha(M)beta(2) (CD11b/CD18) on the surface of conventional DCs (cDCs) and is internalized after binding. Addition of 1C4 inhibited the ability of immature DCs to phagocytose apoptotic cells. 1C4 treatment also partially inhibited the generation of cDCs from bone marrow in the presence of granulocyte macrophage colony-stimulating factor (GM-CSF). Our findings suggest that not only CD11b is involved in the phagocytosis of apoptotic cells, but also that mAb such as 1C4 may be a useful tool for the delivery of specific proteins into the cytoplasm of immature DCs.
    Immunology Letters 10/2008; 120(1-2):42-8.
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    ABSTRACT: SHPS-1 is a transmembrane protein that binds the protein tyrosine phosphatases SHP-1 and SHP-2 and is abundant on the surface of CD11c(+) dendritic cells (DCs). We recently showed that SHPS-1 is essential for priming by DCs of CD4(+) T cells and for development of Th17 cell-mediated experimental autoimmunity. We have now further evaluated the importance of SHPS-1 and that of its ligand CD47 in contact hypersensitivity (CHS) to 2,4-dinitro-1-fluorobenzene (DNFB). Whereas the DNFB-induced CHS response was impaired in mice that express a mutant form of SHPS-1 lacking most of the cytoplasmic region, it was unaffected in CD47-deficient mice. Moreover, treatment of wild-type mice with mAbs to SHPS-1 that either block or do not block the binding of SHPS-1 to CD47 inhibited the CHS response. A mAb to CD47 had no such effect. The 2,4-dinitro-benzenesulfonic acid-induced proliferation of, and production of IFN-gamma or IL-17 by, T cells from DNFB-sensitized wild-type mice were inhibited by either mAb to SHPS-1 but not by that to CD47. In contrast, the blocking mAbs to SHPS-1, but not that to CD47, inhibited an allogeneic mixed leukocyte reaction. Both mAbs to SHPS-1, but not that to CD47, also inhibited the lipopolysaccharide- or polyinosinic-polycytidylic acid-induced production of TNF-alpha by DCs. These results suggest that SHPS-1 is essential for development of CHS, likely as a result of its positive regulation of the priming by DCs of CD4(+) T cells. However, such regulation by SHPS-1 does not appear to require its interaction with CD47.
    Immunology Letters 10/2008; 121(1):52-60.
  • Source
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    ABSTRACT: Although anti-DNA antibodies have been decisively linked to the pathogenesis of lupus nephritis, the mechanisms have not been conclusively determined. Recently, we reported that anti-DNA antibodies may contribute to kidney damage by upregulation of proinflammatory genes in mesangial cells (MC), a process involving both Fc receptor-dependent and independent pathways. In investigating the mechanism by which pathogenic anti-DNA antibodies modulate gene expression in MC, we found that the pathogenic anti-DNA antibody 1A3F bound to high mobility group binding protein 1 (HMGB1), an endogenous ligand for TLR2/4 and RAGE (receptor for advanced glycation end products). Interestingly, HMGB1 treatment of MC induced a similar pattern of genes as stimulation with 1A3F. Furthermore, HMGB1 and 1A3F exhibited a synergistic proinflammatory effect in the kidney, where increased expression of HMGB1 was found in lupus patients but not in patients with other types of renal disease. TLR2/Fc and RAGE/Fc inhibited the proinflammatory effects of 1A3F on MC. Finally, we found enhanced susceptibility of lupus prone MRL-lpr/lpr (MRL/lpr) as compared to normal BALB/c derived MC to pathogenic anti-DNA antibody and LPS stimulation (in particular enhanced chemokine synthesis), in addition to significantly increased expression of TLR4. Our results suggest that gene upregulation in MC induced by nephritogenic anti-DNA antibodies is TLR2/4 and RAGE-dependent. Finally, HMGB1 may act as a proinflammatory mediator in antibody-induced kidney damage in systemic lupus erythematosus (SLE).
    Immunology Letters 10/2008; 121(1):61-73.

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