Immunological investigations (IMMUNOL INVEST)

Publisher: Informa Healthcare

Journal description

Disseminating immunological developments on a worldwide basis, Immunological Investigations encompasses all facets of fundamental and applied immunology, including immunohematology and the study of allergies. This journal provides information presented in the form of original research articles and book reviews, giving a truly in-depth examination of the latest advances in molecular and cellular immunology.

Current impact factor: 1.99

Impact Factor Rankings

2015 Impact Factor Available summer 2016
2014 Impact Factor 1.991
2013 Impact Factor 1.903
2012 Impact Factor 1.731
2011 Impact Factor 1.164
2010 Impact Factor 1.27
2009 Impact Factor 1.466
2008 Impact Factor 1.754
2007 Impact Factor 1.529
2006 Impact Factor 1.276
2005 Impact Factor 0.911
2004 Impact Factor 1.19
2003 Impact Factor 0.886
2002 Impact Factor 1.6
2001 Impact Factor 1.19
2000 Impact Factor 0.635
1999 Impact Factor 1.084
1998 Impact Factor 0.969
1997 Impact Factor 0.787
1996 Impact Factor 0.69
1995 Impact Factor 1.215
1994 Impact Factor 0.968
1993 Impact Factor 0.86
1992 Impact Factor 1.033

Impact factor over time

Impact factor

Additional details

5-year impact 1.63
Cited half-life 5.30
Immediacy index 0.70
Eigenfactor 0.00
Article influence 0.40
Website Immunological Investigations website
Other titles Immunological investigations (Online), Immunological investigations
ISSN 0882-0139
OCLC 48882254
Material type Document, Periodical, Internet resource
Document type Internet Resource, Computer File, Journal / Magazine / Newspaper

Publisher details

Informa Healthcare

  • Pre-print
    • Author can archive a pre-print version
  • Post-print
    • Author cannot archive a post-print version
  • Restrictions
    • 12 months embargo
  • Conditions
    • On author's personal website or institution website
    • Publisher copyright and source must be acknowledged
    • Non-commercial
    • Must link to publisher version
    • Publisher's version/PDF cannot be used
    • NIH funded authors may post articles to PubMed Central for release 12 months after publication
    • Wellcome Trust authors may deposit in Europe PMC after 6 months
  • Classification
    ​ yellow

Publications in this journal

  • [Show abstract] [Hide abstract]
    ABSTRACT: Background and purpose: Some functional limitations and economic burden of therapeutic antibodies indicated that introducing of alternative therapeutic compounds with same or different mechanism of action could be worthwhile. In this regard small-molecule antagonists can have a wide range of impacts, so in this research, we examine prophylactic effects of BIO-1211 [Very Late Antigen-4 (VLA4) blocker), in EAE mouse model of multiple sclerosis in comparison with commercial available medicine, Natalizumab (NTZ). Methods: EAE was induced by subcutaneous immunization of MOG35-55 in 8-week-old C57BL/6 mice. During EAE induction mice separated to distinct groups and received either BIO-1211 (5 and 10 mg/kg) or NTZ (5 mg/kg) and co-administration of this two compounds. After 21 days neuro-inflammatory responses were analyzed using qRT-PCR, western blot, and ELISA methods. Pervade of immune cells to brain was examined by Evans Blue staining and immunohistochemistry (IHC) analysis of specific markers of microglia/monocytes (CD11b), and leukocytes (CD45). Results: Targeted disruption of VLA4/VCAM1 interactions, by BIO-1211 agonist in mice, results in reduced cytokines expression, leukocyte trafficking, and inhibition of inflammatory responses in EAE (P<0.01) in a dose-independent manner (data not shown). Treated mice with both BIO-1211 and NTZ exhibited a considerable depletion in the EAE clinical score which correlated with decreased expression of TNF-α, IL-17, IFN-γ and pervade of CD11b+ and CD45+ cells into the cerebral cortex. Conclusion: Our results indicated that BIO12-11 compound would be useful as a tool to further understand the biological roles of VLA4/VCAM1 interactions and also could consider as EAE prevention agent.
    Immunological investigations 10/2015; 44(7):694-712. DOI:10.3109/08820139.2015.1085391
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    ABSTRACT: The present study was aimed to investigate the anti-arthritic effect of triphala and its underlying mechanism on adjuvant-induced rat model. For comparison purpose, non-steroidal anti-inflammatory drug indomethacin was used. Arthritis was induced by intradermal injection of complete Freund’s adjuvant (0.1 ml) into the right hind paw of the Wistar albino rats. Triphala (100 mg/kg body weight [bwt]) was administered intraperitoneally (from 11th to 20th day) after the arthritis induction. Arthritis induction increased the levels of reactive oxygen species (LPO and NO), elastase, and mRNA expression of pro-inflammatory cytokines (TNF-α, IL-β, IL-17, IL-6 and MCP-1), inflammatory marker enzymes (iNOS and COX-2), receptor activator of nuclear factor kappa-B ligand (RANKL), and transcription factors (NF-kB p65 and AP-1) in the paw tissues of rats. The levels of bone collagen were found to decrease with increased urinary constituents (hydroxyproline and total glycosaminoglycans) in arthritic rats. In addition, the immunohistochemistry analysis revealed increased expression of NF-kBp65 and COX-2 in the paw tissues of arthritic rats. However, administration of triphala significantly inhibited the biochemical and molecular alterations in adjuvant-induced arthritic rats compared to indomethacin (3 mg/kg bwt) as evidenced by the radiological and histopathological analysis. In conclusion, our results suggest that triphala administration ameliorate bone and cartilage degradation during rheumatoid arthritis.
    Immunological investigations 05/2015; 44(4). DOI:10.3109/08820139.2015.1017047
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    ABSTRACT: Background: The strategy of specifically depleting antigen-specific T cells can potentially be used for the treatment of allograft rejection and autoimmunity because it does not suppress the overall immune systems. Methods: In this study, we generated killer polylactic-co-glycolic acid (PLGA) microspheres by covalently coupling major histocompatibility complex (MHC) class I antigens and apoptosis-inducing anti-Fas monoclonal antibody (mAb) onto PLGA microspheres. A modified double-emulsion method was used for the preparation of cell-sized PLGA microspheres. H-2K(b)/peptide monomers were generated in-house and analyzed through flow cytometry. The killer PLGA microspheres were administered intravenously into BALB/c mice (H-2K(d)) that had previously been grafted with skin squares from C57BL/6 mice (H-2K(b)). Tumor cell challenge and third-party mixed lymphocyte culture were used to assess the general immune functions of host. Results: The alloskin graft survival was prolonged by 4 days. The killer PLGA microspheres could specifically deplete the H-2K(b) alloantigen-reactive CD8(+) T cells that infiltrated into the alloskin graft but not CD4(+) T cells, without impairment of host overall immune function. Conclusions: Here, we initially report that PLGA microspheres, which have been widely used as medicine-delivering carriers, were used to prepare antigen-specific killer complexes and treat allograft rejection. Our data highlight the therapeutic potential of this biocompatible and biodegradable antigen-specific killer effector for the treatment of allograft rejection and autoimmune disease.
    Immunological investigations 05/2015; 44(4). DOI:10.3109/08820139.2015.1014098
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    ABSTRACT: Objectives: CTLA-4 exon-1 +49A > G (rs231775) polymorphism has been reported to influence the risk for primary biliary cirrhosis (PBC) as well as type I autoimmune hepatitis (AIH-1) in many studies; however, the results still remain controversial and ambiguous. This study aimed to determine more precise estimations for the relationship between CTLA-4 +49 A > G polymorphism and the risk for PBC and AIH-1 by using a meta-analysis. Design and methods: PubMed, EMBASE and MEDLINE were searched. Odds ratios (ORs) with 95% confidence intervals (CIs) were calculated to estimate the strength of the association. Results: Fifteen studies including 3661 patients with PBC and 4427 controls as well as seven studies including 1270 patients with AIH-1 and 1614 controls were identified. Our pooled analysis revealed that G allele of CTLA-4 gene +49A/G polymorphism may confer an increased risk of PBC in overall (p = 0.001, OR = 1.29; 95% CI = 1.13-1.47) and Caucasians (p = 0.001, OR = 1.32; 95% CI = 1.21-1.44). At genotypic level, the codominant, dominant and recessive models showed no significant association with PBC. With respect to AIH-1, the AG genotype demonstrated a trend for association with increased risk of AIH-1 (p = 0.04, AG vs. AA, OR = 1.20; 95% CI = 1.01-1.43). However, the CTLA-4 alleles as well as genotypes in dominant and recessive models were not associated with a risk for AIH-1 in both Caucasians and Asians. Conclusions: This meta-analysis concluded that the CTLA-4 G allele and the AG genotype were associated with an increased risk for PBC and AIH-1, respectively, suggesting the CTLA-4 +49 A/G polymorphism as a candidate of susceptibility locus to PBC and AIH-1.
    Immunological investigations 05/2015; 44(4). DOI:10.3109/08820139.2014.1003651
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    ABSTRACT: Objective: The aim of this study was to explore whether polymorphisms of intercellular adhesion molecule-1 (ICAM-1) are associated with susceptibility to Crohn's disease (CD) and ulcerative colitis (UC). Methods: The authors conducted a meta-analysis on the associations between the polymorphisms K469E and G241R of ICAM-1 and susceptibility to CD and UC. Results: A total of 8 studies with 801 patients with CD, 672 patients with UC, and 1,828 controls were included in the meta-analysis. The meta-analysis revealed no association between CD and the ICAM-1 469E allele among the subjects (OR = 1.175, 95% CI = 0.901-1.533, p = 0.233). However, stratification by ethnicity indicated an association between the ICAM-1 469E allele and CD in Europeans (OR = 1.425, 95% CI = 1.013-2.002, p = 0.042). Meta-analysis using the homozygosity also showed an association with CD in Europeans (OR = 2.054, 95% CI = 1.036-4.073, p = 0.039). The meta-analysis revealed no association between UC and the ICAM-1 K469E polymorphism. No association between CD or UC and the ICAM-1 G241R polymorphism was observed. Conclusions: This meta-analysis demonstrates that the ICAM-1 K469E polymorphism may be associated with susceptibility to CD in Europeans, but no association was found between ICAM-1 K469E and UC. In contrast, the G241R polymorphism was not found to be associated with susceptibility to either CD or UC.
    Immunological investigations 05/2015; 44(4). DOI:10.3109/08820139.2015.1010685
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    ABSTRACT: Background: Multiple sclerosis (MS) is a progressive inflammatory and neurodegenerative disease of the central nervous system (CNS), the etiology of which is still uncertain. Several case-control studies investigated the association between CD24-P226-C/T polymorphism and MS risk, and these studies have shown inconsistent results. Objective: To address the association of CD24-P226-C/T polymorphism with MS risk by meta-analysis. Methods: A comprehensive search was conducted to identify all eligible studies of CD24-P226-C/T polymorphism and MS risk up to July 2013. The odds ratios (ORs) of CD24 allele distributions in MS were analyzed against controls. Results: In total, seven case-control studies with 949 cases of MS and 1177 controls were included in this meta-analysis. The overall results showed a significant association between CD24-P226-C/T polymorphism and MS susceptibility under homozygote comparison model (OR = 2.496, 95% CI = 1.813–3.435, p < 0.0005), dominant model (OR = 1.367, 95% CI = 1.147–1.629, p < 0.0005), recessive model (OR = 2.305, 95% CI = 1.700–3.126, p < 0.0005) and allelic model (OR = 1.422, 95% CI = 1.244–1.625, p < 0.0005). However, no significant association was observed under heterozygous comparison model (OR = 1.182, 95% CI = 0.982–1.423, p = 0.078). Conclusions: This meta-analysis indicates that CD24 P266-C/T polymorphism is more associated with the risk of MS than healthy controls. However, due to the small sample size in most of the included studies, additional large-scale and well-designed case-control studies were required for the validation of this association.
    Immunological investigations 05/2015; 44(4). DOI:10.3109/08820139.2014.1003650
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    ABSTRACT: Compared to non-sensitized renal transplant recipients, patients with preformed alloantibodies are at greater risk of cellular and humoral rejection and premature graft failure. We explored the effects of adding B-cell depleting agent (rituximab) to standard rabbit anti-thymocyte globulin (rATG) induction regimen for patients with panel reactive antibody levels >50%. Following induction therapy, 14 recipients were given two doses of rituximab (375 mg/m2) within the first month post-transplantation. Their long-term outcomes were compared to a historical control group of 23 recipients who received rATG alone. Graft survival at 5 years was superior with combination therapy compared to induction therapy alone (92.9 versus 48.3%, respectively, p = 0.02). While 30% of the rATG alone group experienced cellular rejection and 26% humoral rejection, none of rituximab plus rATG renal transplant recipients group had rejection. Thus, addition of rituximab to rATG provided superior outcomes to rATG alone. This combination induction therapy should be considered for a high-risk population.
    Immunological investigations 05/2015; 44(4). DOI:10.3109/08820139.2015.1014097
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    ABSTRACT: Exacerbation and relapse of inflammatory bowel disease (IBD) is associated with reduced antibacterial immunity and increased immune regulatory activity, but the source of increased immune regulation during episodes of disease activity is unclear. Myeloid-derived suppressor cells (MDSCs) are a cell type with a well-recognized role in limiting immune reactions. MDSC function in IBD and its relation to disease activity, however, remains unexplored. Here we show that patients with either ulcerative colitis (UC) or Crohn's disease (CD) have high peripheral blood levels of mononuclear MDSCs. Especially exacerbation of disease is associated with higher levels of mononuclear MDSC counts compared with those in remission of disease. Interestingly, chronic experimental colitis in mice coincides with increased MDCS mobilization. Thus, our results suggest that mononuclear MDCS are endogenous antagonists of immune system functionality in mucosal inflammation and the depression of antibacterial immunity associated with exacerbation of disease might involve increased activity of the MDSC compartment.
    Immunological investigations 03/2015; 44(3):1-9. DOI:10.3109/08820139.2014.999937
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    ABSTRACT: This study was conducted to evaluate the adjuvant potential of sulfated Radix Cyathulae officinalis Kuan polysaccharides (sRCPS) and their effects on specific cellular and humoral immune responses to hepatitis B subunit vaccine in mice. Our data demonstrated that sRCPS significantly promoted the rHBsAg-specific IgG, IgG1, IgG2a, and IgG2b antibody titers, the activities of natural killer cells (NK) and cytotoxic T lymphocytes (CTL), T cells proliferation, and phagocytic capacity of peritoneal macrophages. Furthermore, sRCPS increased the levels of IL-4, IL-2, and IFN-γ in CD4(+)T cells and the level of IFN-γ in CD8(+)T cells. In addition, sRCPS enhanced the expression of CD40(+), CD80(+), CD86(+), MHC I and MHC II in dendritic cells (DCs) and upregulated the mRNA levels of MHC I, MHC II. sRCPS downregulated the frequency of CD4(+)CD25(+)Foxp3(+) Treg cells. sRCPS increased both cellular and humoral immune responses by upregulating DC maturation, and suppressing the frequency of Treg cells.
    Immunological investigations 03/2015; 44(3):1-21. DOI:10.3109/08820139.2015.1009546
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    ABSTRACT: Objective: The aim of this study was to determine whether caspase recruitment domain-containing protein 8 (CARD8) rs2043211 polymorphism was associated with susceptibility to inflammatory bowel disease (IBD). Methods: Relevant studies were searched using PubMed and Embase up to February 2014. A meta-analysis was conducted on the association between rs2043211 polymorphism and IBD using: (1) allele contrast, (2) the dominant model, (3) the recessive model, and (4) homozygote contrast. The pooled estimated of risk was obtained by random-effects model or fixed-effects model. Publication bias was assessed by Egger's test. Results: Eight relevant articles with a total of 10 534 IBD patients [6785 Crohn's disease (CD), 3713 ulcerative colitis (UC) and 36 indeterminate colitis (IC)] and 6755 healthy controls were included in the meta-analysis, which consisted of 12 studies, 12 for CD, 10 for UC, 2 for IC. There was no significant association between rs2043211 polymorphism and IBD, CD, and IC in overall population. However, stratified meta-analysis by ethnicity showed significant association between rs2043211 polymorphism and CD in the European population under the dominant model [odds ratio (OR) = 1.210, 95% confidence interval (CI) = 1.013-1.445, p = 0.036] and homozygote contrast (OR = 1.212, 95% CI = 1.005-1.461, p = 0.044). Conclusions: Our meta-analysis results indicated significant association between rs2043211 polymorphism and the susceptibility to CD under the dominant model and homozygote contrast in the European population.
    Immunological investigations 01/2015; 44(3):1-12. DOI:10.3109/08820139.2014.988721
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    ABSTRACT: Given the importance of understanding the genetic variations involved in the pathogenesis of non-Hodgkin's lymphoma (NHL), this pilot study was designed to investigate the impact of CD38 (184C/G; rs6449182) and IL-6 (-174 G/C; rs1800795) gene polymorphism on susceptibility of Egyptians to diffuse large B cell lymphoma (DLBCL); major types of NHL. To the best of our knowledge, this study is the first one that examines CD38 polymorphism in the NHL. Genotyping polymorphism is performed using restriction fragment length polymorphism-polymerase chain reaction (RFLP-PCR) for CD38 and Mutagenically separated PCR (MS-PCR) for IL-6 in 100 Egyptian NHL patients with DLBCL subtype and 119 normal controls. The serum level of IL-6 was measured using Enzyme-linked immunosorbent assay (ELISA). CD38 (184C/G) genotype is significantly increased in NHL patients (p < 0.01), while the GG genotype is significantly increased in controls (p < 0.05). Only two genotypes were found (GG and GC) in IL-6 (-174), no CC in our NHL patients and only one case in the controls. Insignificant change in IL-6 (-174 G/C) genotypes was recorded. Significantly increased serum IL-6 (p < 0.05) was positively correlated (r = 0.17; p < 0.05) with the disease. Taken together, our data stressed the importance of CD38 gene polymorphism in developing DLBCL. Our pilot study indicates that CD38 (184) CG genotype might play a role in DLBCL susceptibility in Egyptians. Additional prospective studies on larger population are needed to confirm our findings.
    Immunological investigations 01/2015; 44(3):1-14. DOI:10.3109/08820139.2014.989328
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    ABSTRACT: Objectives: S100 calcium binding protein A12 (S100A12) has been supposed to be a pro-inflammatory factor associated with non-infectious inflammatory diseases. However, whether S100A12 is involved in the inflammatory process of primary biliary cirrhosis (PBC) has not been shown. Methods: The levels of S100A12 mRNA transcripts in peripheral mononuclear blood cells (PBMCs) of 66 Chinese patients with primary biliary cirrhosis (PBC), 62 healthy controls (HC) and 55 chronic hepatitis B (CHB) were measured by qRT-PCR. S100A12 serum concentrations in 34 PBC patients were measured by ELISA. Results: The levels of S100A12 mRNA transcripts in PBMCs of patients with PBC were significantly higher than healthy controls (p < 0.01) and that of patients with CHB (p < 0.01). Importantly, the levels of S100A12 mRNA in PBMCs and S100A12 protein levels in serum were positively correlated with biochemical indicators of bile duct and hepatocyte damage. Conclusion: S100A12 might participate in the damage of biliary epithelial cells and hepatocytes in PBC, and analysis of S100A12 expression could be useful as a surrogate marker for the evaluation of PBC activity.
    Immunological investigations 10/2014; 44(1):1-10. DOI:10.3109/08820139.2014.914530
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    ABSTRACT: Corneal transplant is the most common solid tissue transplant in humans. Advances in microsurgical techniques, eye banking and the use of corticosteroids have improved the success of corneal transplants. Over 65,000 corneal transplants are being performed worldwide annually. Most of these transplants are performed in developed countries. Cornea is considered an immune privileged site. Despite this, immune mediated graft rejection is the most single cause of cornea graft failure and is one of the major postoperative complications. Incidences from as low as 2% to as high as 50% have been reported depending upon the degree of vascularization. Rejection involves donor tissue recognition and various factors may influence this rejection. Major factors include the antigenic load of the donor tissue; other factors include death to enucleation time, methods and temperature of preserving the tissue. Host factors that may impact the graft include ocular surface diseases such as dry eye, chemical burns and autoimmune diseases such as mucous membrane pemphigoid. Following infection, surgery or trauma, cells of the innate immune system invade the cornea as a result of up-regulation of cytokines, cellular adhesion molecules and growth and angiogenic factors. These factors results in neoangiogenesis and lymphoangiogenesis, leading to immune activation and graft rejection. The various immunological mechanisms that may play a role in the corneal transplant are discussed.
    Immunological investigations 10/2014; 43(8). DOI:10.3109/08820139.2014.910024
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    ABSTRACT: Historically, cellular rather than humoral immunity has gathered the most attention in kidney transplantation. As the specter of cellular acute rejection and early graft loss has faded due to the availability of highly effective immunosuppressive therapy, scientific and clinical studies now focus on improving long-term graft survival. It is increasingly appreciated that alloantibodies directed against HLA and non-HLA antigens are key factors in determining graft longevity. Significant efforts are now being made to better understand the critical impact that B cells and alloantibodies make on organ allocation and graft survival. Future therapies directed specific for the humoral alloresponse will undoubtedly lead to improved outcomes after kidney transplantation. This review will cover some of the advances in the understanding and management of the continuum of humoral immunity in renal transplantation in the pre, peri and post-transplant periods.
    Immunological investigations 10/2014; 43(8). DOI:10.3109/08820139.2014.910016