• Archives of Pharmacal Research
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• v.15 no.1
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• pp.20-29
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• 1992

Effects of squalene on cellular and non-specific immune responses and antitumor activity in mice were investigated. Cellular and non-specific immunological assay parameters adopted in the present study were delayed-type hypersensitivity reaction and resette forming cells (RFC) for cellular immunity, activities of natural killer (NK) cells and phagocyte for non-specific immunity. Squalene resulted in marked increases of cellular and non-specific immune functions and enhancement of host resistance to tumor challenge in dose-dependent manner.

• The Journal of the Korean Society for Microbiology
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• v.16 no.1
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• pp.57-64
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• 1981

The clinical need for agents to modify immune response in the treatment of viral infection has lead to an increased interest in cellular and biochemical mechanisms regulating the immune response and to the development of a variety of biological and chemical substance with immunomodulatory activity. Inosiplex has shown antiviral activity in tissue culture, animal models and huamn studies through augmentation of immune response. However, the effect of inosiplex on immune response in animal has not been extensively analyzed, and the effect of inosiplex on immune response has been paradoxical depending on the time of administration of inosiplex in relation to that of antigen. Therefore, this study was undertaken to assess the effect of inosiplex on the immune response to sheep red blood cells(SRBC) in normal and viral infected mice. Inosiplex increased cellular immune response and plaque forming lymphocyte response to SRBC, decreased the recovery of S. typhimurium from infected mice spleen, and restored the depressed cellular immune response by measle and newcastle disease virus infections. All of the above results were observed only when inosiplex was given after immunization but did not when given before immunization. These results indicate that inosiplex stimulate the efferent are of immune response and may even block the afferent are, and suggest that inosiplex is a very promising drug in therapy of many viral infections.

• Molecules and Cells
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• v.42 no.11
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• pp.747-754
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• 2019

The incidence of atherosclerosis is higher among patients with several autoimmune diseases such as psoriasis, rheumatoid arthritis (RA) and systemic lupus erythematosus (SLE). It is well documented that innate immune cells including macrophages and dendritic cells sense lipid species such as saturated fatty acids and oxidized low-density lipoprotein and produce pro-inflammatory cytokines and chemokines. However, whether a hyperlipidemic environment also impacts autoimmune T cell responses has been unclear. Among $CD4^+$ T cells, Th17 and follicular helper T (Tfh) cells are known to play pathogenic roles in the development of hyperlipidemia-associated autoimmune diseases. This review gives an overview of the cellular and molecular mechanisms by which dysregulated lipid metabolism impacts the pathogenesis of autoimmune diseases, with specific emphasis on Th17 and Tfh cells.

• Asian Pacific Journal of Cancer Prevention
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• v.14 no.6
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• pp.3587-3592
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• 2013

Aims: To study the CIK cell treatment effects on regulation of cellular immune function disorders in patients with lung cancer, and to analyze the time characteristics. Methods: Cellular immune function was assessed by FCM, and patients with functional disorders were randomly divided into two groups, one given CIK cell therapy within 18 months (5 courses) and the other the controls, which were followed up for 1 year with cellular immune functions tested once a month. Results: There were 5 types of cellular immunity, 4 of which are disorders; after CIK treatment, the improvement rate of the 4 groups were 79.1%, 70.8%, 76.0% and 70.0%, intergroup differences not being statistically significant (P=0.675), all significantly higher than in the control group (P=0.000). The median maintenance times for the 4 groups were 10.4 months (9.76-11.04), 8.4 months (7.86-8.94), 9.8 months (9.20-10.4) and 7.9 months (6.25-9.55), respectively. Conclusions: CIK cells were able to improve the immune functions of patients with lung cancer, the rate of improvement and maintenance time being related to the immune function before the treatment and CIK-cell-therapy courses.

• Molecular & Cellular Toxicology
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• v.2 no.4
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• pp.229-235
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• 2006

Volatile organic compounds (VOCs) are a major component of urban air pollution. It is documented that low exposure levels of VOCs induce alterations in immune reactivity resulting in a subsequent higher risk for the development of allergic reactivity and asthma. Despite these facts, there are few reports on the affected primary target and the underlying effective causal mechanisms. So in this study, to better understand the risk of BTX (benzene, toluene and o-xylene) which are the major VOCs and to identify novel biomarkers on immune response to these VOCs exposure in human T lymphocytes, we performed the toxicogenomic study by analyzing of gene expression profiles using 35 k human oligo-microarray. BTX generated specific gene expression patterns in Jurkat cell line. By clustering analysis, we identified some genes as potential markers on immuno-modulating effects of BTX. Four genes of these, HLA-DOA, ITGB2, HMGA2 and 5TAT4 were the most significantly affected by BTX exposure. Thus, this study suggests that these differentially expressed immune genes may play an important role in the pathogenesis on BTX exposure and have significant potential as novel biomarkers of exposure, susceptibility and response to BTC.

• Toxicological Research
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• v.25 no.4
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• pp.159-173
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• 2009

Nuclear factor erythroid derived 2-related factor-2 (Nrf2) is a master transcription regulator of antioxidant and cytoprotective proteins that mediate cellular defense against oxidative and inflammatory stresses. Disruption of cellular stress response by Nrf2 deficiency causes enhanced susceptibility to infection and related inflammatory diseases as a consequence of exacerbated immune-mediated hypersensitivity and autoimmunity. The cellular defense capacity potentiated by Nrf2 activation appears to balance the population of $CD4^+$ and $CD8^+$ of lymph node cells for proper innate immune responses. Nrf2 can negatively regulate the activation of pro-inflammatory signaling molecules such as p38 MAPK, NF-${\kappa}B$, and AP-1. Nrf2 subsequently functions to inhibit the production of pro-inflammatory mediators including cytokines, chemokines, cell adhesion molecules, matrix metalloproteinases, COX-2 and iNOS. Although not clearly elucidated, the antioxidative function of genes targeted by Nrf2 may cooperatively regulate the innate immune response and also repress the expression of pro-inflammatory mediators.

• YAKHAK HOEJI
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• v.46 no.1
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• pp.52-57
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• 2002

Effects of the butanl fraction of Astragali Radix (BFAR) on the cellular and nonspecific immune responses were investigated in ICR mice. Mice were divided into 4 groups and BFAR at doses of 5, 25 and 125 mg/kg u ere administered orally to mice daily for 3 weeks, and the normal animals were given vehicle. The results of this study are summarized as follows; the relative weight of thymus was greatly increased by BFAR treatment, compared with that in mormal mice. However, the body weight gain was not affected. Delayed-type hypersensitivity (DTH) reaction to sheep red blood cells (SRBC) for cellular immunity was significantly enhanced by BFAR treatment, compared with those in normal mice. In these mice, BFAR also dose-dependently increased activities of phagocyte and natural killer (NK) cells as well as the number of leukocyte resulted from nonspecific immunity Thus, these results demonstrate that BFAF treatment results in a significant increase in both cellular and nonspecific immune responses to antigen in concentrations that enhance humoral immune function.

• Journal of Gastric Cancer
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• v.16 no.1
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• pp.1-7
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• 2016

Epstein-Barr virus-associated gastric carcinoma (EBVaGC) is one of the four subtypes of gastric carcinoma (GC), as defined by the novel classification recently proposed by The Cancer Genome Atlas. EBVaGC has several clinicopathological features such as longer survival and higher frequency of lymphoepithelioma-like carcinoma (LELC) and carcinoma with Crohn's disease-like lymphoid reaction that distinguish it from EBV-negative GC. The intensity and pattern of host cellular immune response in GC have been found to significantly correlate with the prognosis of patients with GC, suggesting that immune reaction and tumor microenvironment have critical roles in the progression of GC, and in particular, EBVaGC. Here, we reviewed the cellular and molecular mechanisms underlying prominent immune reactions in patients with EBVaGC. In EBVaGC, deregulation of the expression of immune response-related genes promotes marked intra-or peritumoral immune cell infiltration. The expression of programmed death receptor-ligand 1 is known to be increased in EBVaGC, and therefore, it has been proposed as a favorable prognostic factor for patients with EBVaGC, albeit some data supporting this claim are controversial. Overall, the underlying mechanisms and clinical significance of the host cellular immune response in patients with EBVaGC have not been thoroughly elucidated. Therefore, further research is necessary to better understand the role of tumor microenvironment in EBVaGC.

• BMB Reports
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• v.52 no.2
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• pp.127-132
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• 2019

Cells must fine-tune their gene expression programs for optimal cellular activities in their natural growth conditions. Transcriptional memory, a unique transcriptional response, plays a pivotal role in faster reactivation of genes upon environmental changes, and is facilitated if genes were previously in an active state. Hyper-activation of gene expression by transcriptional memory is critical for cellular differentiation, development, and adaptation. TREM (Transcriptional REpression Memory), a distinct type of transcriptional memory, promoting hyper-repression of unnecessary genes, upon environmental changes has been recently reported. These two transcriptional responses may optimize specific gene expression patterns, in rapidly changing environments. Emerging evidence suggests that they are also critical for immune responses. In addition to memory B and T cells, innate immune cells are transcriptionally hyperactivated by restimulation, with the same or different pathogens known as trained immunity. In this review, we briefly summarize recent progress in chromatin-based regulation of transcriptional memory, and its potential role in immune responses.

• IMMUNE NETWORK
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• v.5 no.1
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• pp.1-10
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• 2005

Background: Chronic infection with hepatitis B virus (HBV) affects about 350 million people worldwide, which have a high risk of development of cirrhosis and hepatocellular carcinoma. Treatment of chronic HBV infection relies on IFN-${\alpha}$ or lamivudine. However, interferon-${\alpha}$ is effective in only about 30% of patients. Also, the occurrence of escape mutations limits the usage of lamivudine. Therefore, the development and evaluation of new compounds or approaches are urgent. Methods: We comparatively evaluated DNA and adenoviral vaccines expressing HBV antigens, either alone or in combined regimens, for their ability to elicit Th1-type immune responses in Balb / c mice which are believed to be suited to resolve HBV infection. The vaccines were tested with or without a genetically engineered IL-12 (mIL-12 N220L) which was shown to enhance sustained Th1-type immune responses in HCV E2 DNA vaccine. Results: Considering the Th1-type cytokine secretion and the IgG2a titers, the strongest Th1-type immune response was elicited by the DNA prime-adenovirus boost regimen in the presence of mIL-12 N220L. In addition, the codelivery of mIL-12 N220L modulated differentially the immune responses by different vaccination regimens. Conclusion: Our results suggest that the DNA prime-adenovirus boost regimen in the presence of mIL-12 N220L may be the best candidate for HBV vaccine therapy of the regimens tested in this study and will be worthwhile being evaluated in chronic HBV patients.