Viral infections in mice with reconstituted human immune system components

Münz, Christian

doi:10.1016/j.imlet.2014.05.012

Cited by 6 publications

(3 citation statements)

References 89 publications

(144 reference statements)

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“…Innate and adaptive immunities, therefore, need to cope with primary and secondary encounters with EBV, in addition to its latency and reactivation. In a minority of infected individuals, EBV is strongly linked to a remarkable variety of nonmalignant and malignant tumors in humans (32). This successful lifelong persistence and, in particular, its ability to establish latency despite specific immune responses show that EBV has developed powerful strategies and mechanisms to exploit, evade, abolish, or downsize effective immune responses to ensure its own survival.…”

Section: Discussionmentioning

confidence: 99%

Viral MicroRNAs Identified in Human Dental Pulp

Zhong

Naqvi

Bair

et al. 2017

Journal of Endodontics

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Introduction MicroRNAs (miRs) are a family of non-coding RNAs that regulate gene expression. They are ubiquitous among multicellular eukaryotes and are also encoded by some viruses. Upon infection, viral miRs (vmiRs) can potentially target gene expression in the host and alter the immune response. While prior studies have reported viral infections in human pulps, the role of vmiRs in pulpal disease is yet to be explored. The purpose of this study was to examine the expression of vmiRs in normal and diseased pulps and to identify potential target genes. Methods Total RNA was extracted and quantified from normal and inflamed human pulps (N=28). Expression profiles of vmiRs were then interrogated using miRNA Microarrays (V3) and the miRNA Complete Labeling and Hyb Kit (Agilent Technologies, Santa Clara, CA). To identify vmiRs that were differentially expressed, we applied a permutation test. Results Of the 12 vmiRs detected in the pulp, 4 vmiRs (including those from herpes virus and human cytomegalovirus) were differentially expressed in inflamed pulps as compared to normal pulps (p<.05). Using bioinformatics we identified potential target genes for the differentially expressed vmiRs. They included key mediators involved in the detection of microbial ligands, chemotaxis, proteolysis, cytokines and signal transduction molecules. Conclusions This data suggests that miRs may play a role in interspecies regulation of pulpal health and disease. Further research is needed to elucidate the mechanisms by which vmiRs can potentially modulate the host response in pulpal disease.

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Section: Discussionmentioning

confidence: 99%

Viral MicroRNAs Identified in Human Dental Pulp

Zhong

Naqvi

Bair

et al. 2017

Journal of Endodontics

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“…A better understanding of the limitations of current models for IVIG will lead to more caution in interpreting preclinical data obtained in mice 17, 39, 60–63 , and to an improved study design of in vivo studies, e.g. with use of humanized mice that are increasingly being used in specific areas of immunology 69, 70 . However, while humanized mice display an interesting alternative to classical mouse models in many immunological aspects, the granulocyte fraction in such models is underrepresented and only accounts for about 3% of the leucocytes 71 , thereby impeding the investigation of neutrophil-driven effects.…”

Section: Discussionmentioning

confidence: 99%

IVIG regulates the survival of human but not mouse neutrophils

Schneider

Wicki

Graeter

et al. 2017

Sci Rep

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Intravenous immunoglobulin (IVIG) are purified IgG preparations made from the pooled plasma from thousands of healthy donors and are being tested in preclinical mouse models. Inherent challenges, however, are the pluripotency of IVIG and its xenogeneicity in animals. IVIG can alter the viability of human neutrophils via agonistic antibodies to Fas and Siglec-9. In this study, we compared the effects of IVIG on human and mouse neutrophils using different death assays. Different commercial IVIG preparations similarly induced cytokine-dependent death in human neutrophils, whereas they had no effects on the survival of either peripheral blood or bone marrow neutrophils from C57BL/6 or BALB/c mice. F(ab’)2 but not Fc fragments of IVIG induced death of human neutrophils, whereas neither of these IVIG fragments, nor agonistic monoclonal antibodies to human Fas or Siglec-9 affected the viability of mouse neutrophils. Pooled mouse IgG, which exhibited a different immunoprofile compared to IVIG, also had no effect on mouse cells. Together, these observations demonstrate that effects of IVIG on neutrophil survival are not adequately reflected in current mouse models, despite the key role of these cells in human inflammatory and autoimmune diseases.

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“…Valuable information on the immune response to EBV has been gained from studies on related murine or rhesus macaque-specific herpesviruses in their respective hosts (Stevenson et al 2009;Wang 2013). Mice with humanized immune system components (HIS mice) provide a valuable alternative, recapitulating several important aspects of EBV-specific immunity (Chatterjee et al 2014;Munz 2014;Strowig et al 2009;Traggiai et al 2004). Future infection studies with mutant EBV strains in these model systems will provide important information on the contribution of immune evasion strategies to viral infection and pathogenesis.…”

Section: Conclusion and Future Perspectivesmentioning

confidence: 99%

Immune Evasion by Epstein-Barr Virus

Ressing

Gent

Gram

et al. 2015

Epstein Barr Virus Volume 2

103

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Epstein-Bar virus (EBV) is widespread within the human population with over 90% of adults being infected. In response to primary EBV infection, the host mounts an antiviral immune response comprising both innate and adaptive effector functions. Although the immune system can control EBV infection to a large extent, the virus is not cleared. Instead, EBV establishes a latent infection in B lymphocytes characterized by limited viral gene expression. For the production of new viral progeny, EBV reactivates from these latently infected cells. During the productive phase of infection, a repertoire of over 80 EBV gene products is expressed, presenting a vast number of viral antigens to the primed immune system. In particular the EBV-specific CD4+ and CD8+ memory T lymphocytes can respond within hours, potentially destroying the virus-producing cells before viral replication is completed and viral particles have been released. Preceding the adaptive immune response, potent innate immune mechanisms provide a first line of defense during primary and recurrent infections. In spite of this broad range of antiviral immune effector mechanisms, EBV persists for life and continues to replicate. Studies performed over the past decades have revealed a wide array of viral gene products interfering with both innate and adaptive immunity. These include EBV-encoded proteins as well as small noncoding RNAs with immune-evasive properties. The current review presents an overview of the evasion strategies that are employed by EBV to facilitate immune escape during latency and productive infection. These evasion mechanisms may also compromise the elimination of EBV-transformed cells, and thus contribute to malignancies associated with EBV infection.

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Viral infections in mice with reconstituted human immune system components

Cited by 6 publications

References 89 publications

Viral MicroRNAs Identified in Human Dental Pulp

Viral MicroRNAs Identified in Human Dental Pulp

IVIG regulates the survival of human but not mouse neutrophils

Immune Evasion by Epstein-Barr Virus

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