• Journal of electromagnetic engineering and science
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• v.13 no.1
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• pp.54-61
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• 2013

An equivalent model has been developed to estimate the electromagnetic immunity for integrated circuits under a complex electromagnetic environment. The complete model is based on the characteristics of the equipment and physical configuration of the device under test (DUT) and describes the measurement setup as well as the target integrated circuits under test, the corresponding package, and a specially designed printed circuit board. The advantage of the proposed model is that it can be applied to a SPICE-like simulator and the immunity of the integrated circuits can be easily achieved without costly and time-consuming measurements. After simulation, measurements were performed to verify the accuracy of the equivalent model for immunity prediction. The improvement of measurement accuracy due to the added effect of a bi-directional coupler in the test setup is also addressed.

• Clinical and Experimental Pediatrics
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• v.48 no.11
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• pp.1153-1161
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• 2005

As known by other name(natural immunity), the innate immune system comprises all those mechanisms for dealing with infection that are constitutive or built in, changing little with age or with experience of infection. Though in some ways less sophisticated than adaptive immunity, innate immunity should not belittled, since it has evidently protected thousands of species of invertebrates sufficiently to survive for up to 2 billion years. In the innate immune system, molecules of both cellular and humoral types are involved, corresponding to the need to recognize and dispose of different types of pathogen, to promote inflammatory responses and to interact to the adaptive immune system. A major features of innate immunity are the presence of the normal gut flora, complements, macrophages, dendritic cells, natural killer cells and many cytokines that can block the establishment of infection. Both phagocytic cells and complement system have tremendous potential for damaging host cells, but fortunately they are normally only triggered by foreign materials, and usually most of their destructive effects are focussed on the surface of these or in the safe environment of the phagolysosome. This article addreses the comprehensive mechanisms of the major components of the innate immune system to prevent the infection.

• Journal of Microbiology and Biotechnology
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• v.26 no.2
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• pp.432-439
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• 2016

Shiga toxins (Stxs) produced by Shiga toxin-producing Escherichia coli (STEC) strains are major virulence factors that cause fatal systemic complications, such as hemolytic uremic syndrome and disruption of the central nervous system. Although numerous studies report proinflammatory responses to Stx type 1 (Stx1) or Stx type 2 (Stx2) both in vivo and in vitro, none have examined dynamic immune regulation involving cytokines and/or unknown inflammatory mediators during intoxication. Here, we showed that enzymatically active Stxs trigger the dissociation of lysyl-tRNA synthetase (KRS) from the multi-aminoacyl-tRNA synthetase complex in human macrophage-like differentiated THP-1 cells and its subsequent secretion. The secreted KRS acted to increase the production of proinflammatory cytokines and chemokines. Thus, KRS may be one of the key factors that mediate transduction of inflammatory signals in the STEC-infected host.

• IMMUNE NETWORK
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• v.13 no.6
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• pp.249-256
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• 2013

How Th2 immunity develops in vivo remains obscure. Basophils have been considered key innate cells producing IL-4, a cytokine essential for Th2 immunity. Increasing evidence suggests that basophils are dispensable for the initiation of Th2 immunity. In this study, we revisited the role of basophils in Th2 immune responses induced by various types of adjuvants. Mice deficient in IL-3 or IL-3 receptor, in which basophil lymph node recruitment is completely abolished, fully developed wild type level Th2 CD4 T cell responses in response to parasite antigen or papain immunization. Similar finding was also observed in mice where basophils are inducibly ablated. Interestingly, IL-4-derived from non-T cells appeared to be critical for the generation of IL-4-producing CD4 T cells. Other Th2 promoting factors including IL-25 and thymic stromal lymphopoietin (TSLP) were dispensable. Therefore, our results suggest that IL-3- and basophil-independent in vivo Th2 immunity develops with the help of non-T cell-derived IL-4, offering an additional mechanism by which Th2 type immune responses arise in vivo.

• Molecules and Cells
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• v.46 no.11
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• pp.710-724
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• 2023

The plant defense responses to microbial infection are tightly regulated and integrated with the developmental program for optimal resources allocation. Notably, the defense-associated hormone salicylic acid (SA) acts as a promoter of flowering while several plant pathogens actively target the flowering signaling pathway to promote their virulence or dissemination. Ralstonia pseudosolanacearum inject tens of effectors in the host cells that collectively promote bacterial proliferation in plant tissues. Here, we characterized the function of the broadly conserved R. pseudosolanacearum effector RipL, through heterologous expression in Arabidopsis thaliana. RipL-expressing transgenic lines presented a delayed flowering, which correlated with a low expression of flowering regulator genes. Delayed flowering was also observed in Nicotiana benthamiana plants transiently expressing RipL. In parallel, RipL promoted plant susceptibility to virulent strains of Pseudomonas syringae in the effector-expressing lines or when delivered by the type III secretion system. Unexpectedly, SA accumulation and SA-dependent immune signaling were not significantly affected by RipL expression. Rather, the RNA-seq analysis of infected RipL-expressing lines revealed that the overall amplitude of the transcriptional response was dampened, suggesting that RipL could promote plant susceptibility in an SA-independent manner. Further elucidation of the molecular mechanisms underpinning RipL effect on flowering and immunity may reveal novel effector functions in host cells.

• ETRI Journal
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• v.19 no.4
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• pp.389-401
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• 1997

In this paper, we consider the relationship between nonlinearity and correlation immunity of Boolean functions. In particular, we discuss the nonlinearity of correlation immune functions suggested by P. Camion et al. For the analysis of such functions, we present a simple method of generating the same set of functions, which makes it possible to construct correlation immune functions with controllable correlation immunity and nonlinearity. Also, we find a bound for the correlation immunity of functions having maximal nonlinearity.

• Korean Journal of Agricultural Science
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• v.35 no.2
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• pp.177-182
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• 2008

Type I Interferons (IFNs) are potent antiviral cytokines that modulate both innate immunity and adaptive immunity. Type I IFNs are immediately induced by viral infection, and stimulate production of a broad range of gene products such as double-stranded RNA-activated protein kinase (PKR), 2' 5'-oligoadenylate synthetase (OAS)/RNaseL and Mx GTPases. These proteins inhibit viral replication in host cells. Type I IFNs, in turn, lead to antiviral state at early phase of viral infection. We provide an overview of the knowledge of IFN-inducible antiviral proteins conserved in vertebrates.

• Proceedings of the PSK Conference
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• 2002.10a
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• pp.310.2-310.2
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• 2002

Macrophage activated by LPS/IFN-${\gamma}$ playa important role in imflammation. innate immunity and tumor immunity. The recent report has indicated that LPS treated bone marrow macrophages were induced apoptosis. but IFN-${\gamma}$ protects from apoptosis induced by several stimuli in complete medium condition (Jordi et al.. Immunity. Vo1.11. 103-113. 1999). (omitted)

• IMMUNE NETWORK
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• v.11 no.5
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• pp.245-252
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• 2011

Antimicrobial peptides/proteins are ancient and naturally-occurring antibiotics in innate immune responses in a variety of organisms. Additionally, these peptides have been recognized as important signaling molecules in regulation of both innate and adaptive immunity. During mycobacterial infection, antimicrobial peptides including cathelicidin, defensin, and hepcidin have antimicrobial activities against mycobacteria, making them promising candidates for future drug development. Additionally, antimicrobial peptides act as immunomodulators in infectious and inflammatory conditions. Multiple crucial functions of cathelicidins in antimycobacterial immune defense have been characterized not only in terms of direct killing of mycobacteria but also as innate immune regulators, i.e., in secretion of cytokines and chemokines, and mediating autophagy activation. Defensin families are also important during mycobacterial infection and contribute to antimycobacterial defense and inhibition of mycobacterial growth both in vitro and in vivo. Hepcidin, although its role in mycobacterial infection has not yet been characterized, exerts antimycobacterial effects in activated macrophages. The present review focuses on recent efforts to elucidate the roles of host defense peptides in innate immunity to mycobacteria.

• IMMUNE NETWORK
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• v.9 no.6
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• pp.209-235
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• 2009

There has been an explosion of literature focusing on the role of regulatory T (Treg) cells in cancer immunity. It is becoming increasingly clear that Treg cells play an active and significant role in the progression of cancer, and have an important role in suppressing tumor-specific immunity. Thus, there is a clear rationale for developing clinical strategies to diminish their regulatory influences, with the ultimate goal of augmenting antitimor immunity. Therefore, manipulation of Treg cells represent new strategies for cancer treatment. In this Review, I will summarize and review the explosive recent studies demonstrating that Treg cells are increased in patients with malignancies and restoration of antitumor immunity in mice and humans by depletion or reduction of Treg cells. In addition, I will discuss both the prognostic value of Treg cells in tumor progression in tumor-bearing hosts and the rationale for strategies for therapeutic vaccination and immunotherapeutic targeting of Treg cells with drugs and microRNA.