• IMMUNE NETWORK
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• 제14권4호
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• pp.187-200
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• 2014

Herpes simplex virus types 1 and 2 (HSV-1 and HSV-2) are the most common cause of genital ulceration in humans worldwide. Typically, HSV-1 and 2 infections via mucosal route result in a lifelong latent infection after peripheral replication in mucosal tissues, thereby providing potential transmission to neighbor hosts in response to reactivation. To break the transmission cycle, immunoprophylactics and therapeutic strategies must be focused on prevention of infection or reduction of infectivity at mucosal sites. Currently, our understanding of the immune responses against mucosal infection of HSV remains intricate and involves a balance between innate signaling pathways and the adaptive immune responses. Numerous studies have demonstrated that HSV mucosal infection induces type I interferons (IFN) via recognition of Toll-like receptors (TLRs) and activates multiple immune cell populations, including NK cells, conventional dendritic cells (DCs), and plasmacytoid DCs. This innate immune response is required not only for the early control of viral replication at mucosal sites, but also for establishing adaptive immune responses against HSV antigens. Although the contribution of humoral immune response is controversial, $CD4^+$ Th1 T cells producing IFN-${\gamma}$ are believed to play an important role in eradicating virus from the hosts. In addition, the recent experimental successes of immunoprophylactic and therapeutic compounds that enhance resistance and/or reduce viral burden at mucosal sites have accumulated. This review focuses on attempts to modulate innate and adaptive immunity against HSV mucosal infection for the development of prophylactic and therapeutic strategies. Notably, cells involved in innate immune regulations appear to shape adaptive immune responses. Thus, we summarized the current evidence of various immune mediators in response to mucosal HSV infection, focusing on the importance of innate immune responses.

• 대한간호학회지
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• 제44권4호
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• pp.446-457
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• 2014

Purpose: This study was done to evaluate the effects of psychosocial interventions on cortisol and immune response in adult patients with cancer. Methods: MEDLINE via PubMed, Cochrane Library CENTRAL, EMBASE, CINAHL and domestic electronic databases were searched. Twenty controlled trials (11 randomized and 9 non-randomized trials) met the inclusion criteria with a total of 862 participants. Methodological quality was assessed using the Cochrane's Risk of Bias for randomized studies and the Risk of Bias Assessment tool for non randomized studies. Data were analyzed using the RevMan 5.2.11 program of Cochrane library. Results: Overall, study quality was moderate to high. The weighted average effect size across studies was -0.32 (95% CI [-0.56, -0.07], p=.010, $I^2 $=45%) for cortisol concentration, -0.62 (95%CI [-0.96,-0.29], p<.001, $I^2 $=0%) for T lymphocyte (CD3) and -0.45 (95%CI [-0.74, -0.16], p=.003, $I^2 $=0%) for Th lymphocyte (CD4) numbers. Psychosocial interventions were not effective for Tc lymphocyte (CD4), NK cell, monocyte, and cytokine response. Conclusion: Although these results provide only small evidence of successful immune modulation, they support the conclusion that psychosocial interventions can assist cancer patients in reducing emotional distress and improving immune response.

• BMB Reports
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• 제38권2호
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• pp.253-257
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• 2005

In our previous study, Soamsan, a traditional Oriental medicine, was shown to enhance the induction of antigen-specific immune responses, and it was speculated that the enhancing activity might be closely associated with glycoproteins contained within the medicine. To elucidate this speculation, protein samples from each component, used in the preparation of Soamsan, were obtained and their immune stimulating activities were tested with mouse splenocytes. All the samples markedly enhanced the lymphocyte proliferation and cytokine secretion by the mouse splenocytes. In particular, the enhancement was significantly higher with the protein sample treatments than with those of the original crude sample. Furthermore, the pronase E- and $NaIO_4$-mediated inhibition of splenocyte-stimulation activity of the protein samples clearly supported that glycoproteins are the main class of active ingredients responsible for the lymphocyte stimulating activity of the samples. Consequently, our findings suggest that glycoproteins might have a pivotal role in Soamsan-mediated immune modulation, although the in vivo effect of the glycoproteins should be further elucidated.

• Journal of Communications and Networks
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• 제13권5호
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• pp.442-448
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• 2011

It's a challenging task to design a high performance modulation for satellite and space communications due to the limited power and bandwidth resource. Constant envelope modulation is an attractive scheme to be used in such cases for their needlessness of input power back-off about 2~3 dB for avoidance of nonlinear distortion induced by high power amplifier. The envelope of Feher quadrature phase shift keying (FQPSK) has a least fluctuation of 0.18 dB (quasi constant envelope) and can be further improved. This paper improves FQPSK by defining a set of new waveform functions, which changes FQPSK to be a strictly constant envelope modulation. The performance of the FQPSK adopting new waveform is justified by analysis and simulation. The study results show that the novel FQPSK is immune to the impact of HPA and outperforms conventional FQPSK on bit error rate (BER) performance. The BER performance of this novel modulation is better than that of FQPSK by more than 0.5 dB at least and 2 dB at most.

• IMMUNE NETWORK
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• 제13권5호
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• pp.163-167
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• 2013

The dynamics of the virus-host interface in the response to respiratory virus infection is not well-understood; however, it is at this juncture that host immunity to infection evolves. Respiratory viruses have been shown to modulate the host response to gain a replication advantage through a variety of mechanisms. Viruses are parasites and must co-opt host genes for replication, and must interface with host cellular machinery to achieve an optimal balance between viral and cellular gene expression. Host cells have numerous strategies to resist infection, replication and virus spread, and only recently are we beginning to understand the network and pathways affected. The following is a short review article covering some of the studies associated with the Tripp laboratory that have addressed how respiratory syncytial virus (RSV) operates at the virus-host interface to affects immune outcome and disease pathogenesis.

• 식품과학과 산업
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• 제55권3호
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• pp.264-275
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• 2022

The regulation of macrophages is a major target for dietary immune modulation for their involvement in both innate and adoptive immune responses. Studies revealed that macrophages are unique in their plasticity to polarize into either inflammatory M1 subset or anti-inflammatory M2 cells. Recently, cellular energy metabolism including both glycolysis and oxidative phosphorylation is demonstrated to control macrophage dichotomy. In this review, the differential utilization of glucose, lipids, amino acids, and irons by M1 and M2 cells are discussed in detail. In addition, several dietary approaches for the alteration of inflammatory M1 cells to M2 phenotypes are reviewed for development of functional foods for immune regulation.

• Molecules and Cells
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• 제45권8호
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• pp.513-521
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• 2022

Cytotoxic T lymphocyte antigen-4 (CTLA-4) is an immune checkpoint molecule that is mainly expressed on activated T cells and regulatory T (Treg) cells that inhibits T-cell activation and regulates immune homeostasis. Due to the crucial functions of CTLA-4 in T-cell biology, CTLA-4-targeted immunotherapies have been developed for autoimmune disease as well as cancers. CTLA-4 is known to compete with CD28 to interact with B7, but some studies have revealed that its downstream signaling is independent of its ligand interaction. As a signaling domain of CTLA-4, the tyrosine motif plays a role in inhibiting T-cell activation. Recently, the lysine motif has been shown to be required for the function of Treg cells, emphasizing the importance of CTLA-4 signaling. In this review, we summarize the current understanding of CTLA-4 biology and molecular signaling events and discuss strategies to target CTLA-4 signaling for immune modulation and disease therapy.

• 한국미생물학회:학술대회논문집
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• 한국미생물학회 2004년도 International Meeting of the Microbiological Society of Korea
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• pp.97-97
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• 2004

• 대한약학회:학술대회논문집
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• 대한약학회 2001년도 Proceedings of International Convention of the Pharmaceutical Society of Korea
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• pp.151.2-152
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• 2001

• IMMUNE NETWORK
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• 제15권2호
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• pp.83-90
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• 2015

Evaluation and screening of vaccines against tuberculosis depends on development of proper cost effective disease models along with identification of different immune markers that can be used as surrogate endpoints of protection in preclinical and clinical studies. The objective of the present study was therefore evaluation of subcutaneous model of M.tuberculosis infection along with investigation of different immune biomarkers of tuberculosis infection in BALB/c mice. Groups of mice were infected subcutaneously with two different doses : high ($2{\times}10^6CFU$) and low doses ($2{\times}10^2CFU$) of M.tuberculosis and immune markers including humoral and cellular markers were evaluated 30 days post M.tuberculosis infections. Based on results, we found that high dose of subcutaneous infection produced chronic disease with significant (p<0.001) production of immune markers of infection like $IFN{\gamma}$, heat shock antigens (65, 71) and antibody titres against panel of M.tuberculosis antigens (ESAT-6, CFP-10, Ag85B, 45kDa, GroES, Hsp-16) all of which correlated with high bacterial burden in lungs and spleen. To conclude high dose of subcutaneous infection produces chronic TB infection in mice and can be used as convenient alternative to aerosol models in resource limited settings. Moreover assessment of immune markers namely mycobacterial antigens and antibodies can provide us valuable insights on modulation of immune response post infection. However further investigations along with optimization of study protocols are needed to justify the outcome of present study and establish such markers as surrogate endpoints of vaccine protection in preclinical and clinical studies in future.