• Korean Journal of Microbiology
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• v.47 no.4
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• pp.342-347
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• 2011

T cells play a key role in viral infection. However, in patients with chronic hepatitis C virus (HCV) infection, HCV-specific T cells are dysfunctional and impaired in the liver, which is the primary site for HCV replication. There are multiple potential mechanisms for HCV-specific T cell dysfunction including induction of immune inhibitory pathways (program death-1; PD-1, cytotoxic t lymphocyte associated antigen-4; CTLA-4) and immune tolerance induced specific for the liver. However, the interaction between hepatocytes and HCV-specific CD8 T cells has not clearly established. In this study, we confirmed huh (human hepatoma) 7.5 cells expressing HLA (human leukocyte antigen) A2 presented antigen to activate HCV-specific CD8 T cells in HLA A2-restricted manner and expression of PD-L (program death ligand) 1 on huh7.5 cells reduced HCV-specific CD8 T cell activation, suggesting an immune modulatory activity. Loss of HCV-specific tetramer responses following antigenic stimulation correlated with increased caspase-3 activity. In addition, PD-L1 on huh7.5 cells rescued HCV-specific CD8 T cells from apoptosis. Our results suggest that the interaction between PD-L1 and PD-1 can recover the function of HCV-specific CD8 T cells in the liver, which could be applied in therapy of HCV chronic infection.

• Journal of Life Science
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• v.25 no.12
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• pp.1425-1431
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• 2015

The lymphocyte component of the immune system is divided into B lymphocytes and T lymphocytes. B lymphocytes produce antibodies (humoral immunity) via maturation into plasma cells, and T lymphocytes kill other cells or organisms (cellular immunity). A traditional immunological paradigm is that B lymphocyte and T lymphocyte interactions are a one-way phenomenon, with T lymphocytes helping to induce the terminal differentiation of B lymphocytes into immunoglobulin class-switched plasma cells. A deficiency of T lymphocytes was reported to result in defective B lymphocyte function. However, evidence for a reciprocal interaction between B and T lymphocytes is emerging, with B lymphocytes influencing the differentiation and effector function of T lymphocytes. For example, B lymphocytes have been shown to induce direct tolerance of antigen-specific CD8⁺ T lymphocytes and induce T lymphocytes anergy via transforming growth factor-beta (TGF-β) production. The present study showed that LPS-stimulated B lymphocytes inhibited the differentiation of Th1 lymphocytes by inhibiting the production of interleukin-12 (IL-12) from dendritic cells. An interaction between the B lymphocytes and dendritic cells was not needed for this inhibition, and the B lymphocytes did not alter dendritic cell maturation. B lymphocyte-derived soluble factor (BDSF) suppressed the LPS-induced IL-12p35 transcription in the dendritic cells. Overall, these results point to a novel B lymphocyte- mediated immune suppressive mechanism. The findings cast doubt on the traditional paradigm of immunological interactions involving B lymphocyte and T lymphocyte interactions.

• The Journal of Dong Guk Oriental Medicine
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• v.7 no.1
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• pp.33-41
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• 1998

Lymph node tissues of BALB/C mouse treated with DNCB were immunohistochemically observed to investigate the activation of cell mediated immunity in lymph node of murine with allergic contact dermatitis. The inguinal region of BALB/C mice were sensitized by one application of $25{\mu}l$ of 5% 2,4-dinitrochlorobenzene(DNCB) onto an abdominal skin and 2 weeks later, the mice were challenged with $4{\mu}l$ of 2.5% DNCB. The inguinal lymph node were obtained at hour 24, 48, and 72 after 2nd DNCB treatment and embedded with paraffin, and then stained by following ABC method that used monoclonal antibody including L3T4(CD4), Ly2(CD8), IL-2R(CD25). The distribution of helper T lymphocytes, cytotoxic T lymphocytes and IL-2 receptors began to increase at hour 24 after after 2nd DNCB treatment and these increase appeared in paracortical area and medullary sinius. These increase were greatest at hour 48. These results indicated that the IL-2 secretion began to increase by activation of helper T lymphocytes in lymph node of DNCB re-exposure area and subsequently to activate suppress T lymphocytes.

• Korean Journal of Microbiology
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• v.50 no.2
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• pp.169-172
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• 2014

Recently, Hepatitis C virus (HCV) replication system has been established using human hepatoma cells (huh cell) and a variety of HCV clones. In this study, we established an infectious HCV replication system using huh7.5 cells and J6/JFH1 clone (genotype 2a). In addition, we investigated the antigen presentation capability of HCV-infected huh7.5 cells to HCV-specific T cells. Interestingly, HCV-infected huh7.5 cells were not capable of activating HCV-specific T cells. However, huh7.5 cells stimulated by exogenous HCV peptide were able to activate HCV-specific T cells, which was shown to produce TNF-${\alpha}$ and IFN-${\gamma}$. We further examined if HCV infection has an inhibitory effect on the expression of MHC class I molecule of huh7.5 cells. We found that HCV infection did not change the expression level of MHC class I molecule on huh7.5 cells.

• The Journal of Dong Guk Oriental Medicine
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• v.6 no.2
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• pp.99-107
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• 1998

Cyclosporin A(CsA) is a selective immunosuppressive agent that has been credited with improved survival of solid organ allografts. Lymph node of BALB/C mouse administered CsA immunohistochemically observed to understand immunosuppressive effects of CsA on T lymphocytes, IL-2 receptors, and natural killer NK cells in lymph node. CsA orally administered daily for 10days at the dose 45mg/kg/day/. The lymph node were obtained at day 3, 7, and 14 after CsA administration and embedded with paraffin, and then stained by following ABC method that used monoclonal antibody including L3T4(CD4), Ly2(CD8), IL-2R(CD25), and NK-1.1(CD56). There were little changes of reactive degree and number of helper T lymphocytes, cytotoxic T lymphocytes, IL-2 receptors, and NK cells at day 3 after CsA administration, but they began to decrease at day 7. These decrease were greatest at day 14. The helper T lymphocytes. cytotoxic T lymphocytes, IL-2 receptors, and NK cells distributed in paracortex and medullary sinus. These results indicated that the secretion of IL-2 began to decrease at day 7 after CsA administration and subsequently to suppress T lymphocytes and NK cell as components of cell-mediated immunity.

• Journal of the Korean Society of Radiology
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• v.13 no.1
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• pp.133-140
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• 2019

Triglycerides (TG) are one of the triggers of chronic inflammatory lesions in the blood vessels. In the key factors in the development of inflammatory diseases, Pro-inflammatory cytokines such as tumor necrosis factor-alpha $(TNF-){\alpha}$ and interleukin-1 beta ($IL-1{\beta}$) contribute to the development of inflammatory lesions by recruiting other immune cells in the inflamed area or causing cell necrotic death. In this study, I investigated the effect of Jurkat T lymphocytes and U937 monocytes involved in vascular inflammation development on the expression of $TNF-{\alpha}$ and $IL-1{\beta}$ on exposure to TGs. In Jurkat cells, mRNA expression of $TNF-{\alpha}$ is increased by exposure to TGs. However, the expression levels of $TNF-{\alpha}$ and $IL-1{\beta}$ were increased by TGs in U937 cells. To investigate whether inducible nitric oxide synthase (iNOS) is involved in the increase of expression of $TNF-{\alpha}$ and $IL-1{\beta}$ by TGs, treatment of W1400 (an iNOS inhibitor) resulted in recovery of expression level both $TNF-{\alpha}$ and $IL-1{\beta}$. Based on the present study, it was confirmed that the expression of $TNF-{\alpha}$ and $IL-1{\beta}$ in monocytes and T lymphocytes. This increased cytokines contribute to development of vascular inflammatory lesions. In addition, iNOS is involved in the increase of $TNF-{\alpha}$ and $IL-1{\beta}$ expression by TGs.

• Clinical and Experimental Reproductive Medicine
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• v.37 no.3
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• pp.231-237
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• 2010

Objective: To evaluate whether T helper 1 (Th1) immune response is predominant in women with reproductive failures (recurrent spontaneous abortion and recurrent implantation failure) and the activation of T cell is related to Th1 propensity. Methods: Women with a history of recurrent implantation failure or recurrent spontaneous abortion comprise the study group (n=37). Controls are normal fertile women without a history of infertility or pregnancy losses (n=11). Th1/Th2 ratios of interferon (INF)-$\gamma$/interleukin (IL)-10 and tumor necrosis factor (TNF)-$\alpha$/IL-10 expression on $CD3^+/4^+$ cells, CD154, and CD69 expression on T cells are measured by flow cytometric analysis. Results: The ratios of TNF-$\alpha$ to IL-10 expressing on $CD3^+/4^+$ cells (Th1/Th2 cell ratios) are significantly higher in study group ($42.1{\pm}2.3$) as compared with that of controls ($28.7{\pm}2.7$) (p=0.002). The overall trend of CD154 and CD69 expression on T cells are elevated in study group than those of controls. The proportion (%) of $CD3^+/4^+/154^+$ cells ($1.7{\pm}0.5$ vs. $0.3{\pm}0.2$, p=0.038) and the % of $CD3^+/8^+/154^+$ cells ($0.6{\pm}0.2$ vs. $0.1{\pm}0.0$, p=0.024) are significantly higher in study group. The % of $CD3^+/69^+$ cells ($5.6{\pm}1.9$ vs. $1.3{\pm}5.4$, p=0.046) and % of $CD3^+/8^+/69^+$ cells ($4.8{\pm}1.3$ vs. $1.8{\pm}0.2$, p=0.035) among $CD3^+/8^+$ cells are significantly increased in study group. Conclusion: Women with reproductive failures have Th1 propensity with increased T cell activation. These finding means that activated T cell has a harmful effect on early pregnancy and implantation by induction of Th1 immunity.

• Journal of Life Science
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• v.22 no.3
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• pp.312-317
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• 2012

The time-dependent effects of highly intensive exercise on the hematological properties of leukocytes, as well as $CD4^+$ and $CD8^+$ level changes as T-lymphocyte activation subsets and the cell death of lymphocytes in rats were studied in this research. Twenty, 60, and 120 min of highly intensive exercise was performed daily for 8 weeks. Total leukocyte counts in the blood of rats exercising for 20 min were elevated; they then decreased to less than the level of the control group up to 120 min. The patterns of lymphocyte level changes were directly influenced by exercise duration and the extents of alteration were similar to the total leukocytes counts. The levels of $CD4^+$ and $CD8^+$ in the blood of the exercising rats were not statistically different even when the exercise was continued for 120 min; thus, the exercise did not affect T-lymphocyte activation. Early- and late-stage lymphocyte apoptosis was not affected by the length of exercise, except that late-phase apoptosis was slightly increased at 120 min, suggesting that aging processes for lymphocyte apoptosis might be stimulated at that time. As the exercise time became longer, stimulated necrosis of lymphocytes was observed, so damage in lymphocytes and a potential loss of immunity might be presumed. The current observation suggests that long-term, highly intensive exercise might result in a loss of immunity that could be due to the damage of lymphocytes in terms of both their numbers and inflammation-related functions. The results suggest that under highly intensive exercise conditions, more than 20 min of exercise should not be suggested for health care purposes.

• The Korean Journal of Pharmacology
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• v.29 no.1
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• pp.121-130
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• 1993

This study was done to classify the proteins involved in the specific phosphorylation using the rat peripheral blood lymphocytes (rPBL) stimulated with mitogens, phorbol 12-myristate 13-acetate (PMA) and concanavalin A (Con A). The lymphocytes were incubated with $^{32}P-orthophosphate$ before PMA or Con A stimulation. The migration patterns of the phosphorylated proteins of mitogen-treated rPBL in two dimensional electrophoretic fields were analyzed after autoradiography. The stimulation of the lymphocytes with PMA and Con A increased the phosphorylation of thirteen protein fractions. The phosphorylation intensities of the protein spots differ to the treatments of the cells with specific kinase inhibitors, H-7 and W-7. These protein fractions were grouped into 3 classes, namely, PKC-mediated, CaM kinase-mediated, and other kinase mediated proteins. The effect of the duration of the stimulation on the phosphorylated behaviors occurred concurrently, not sequentially, although each individual protein fraction had a different time for the peak phosphorylation during the stimulation period upto 30 minutes. The phosphoproteins found in the cytosolic soluble fraction were phosphorylated prior to those in the pellet, whose phosphorylations were sustained at a high level for over 10 minutes. The above results suggest that the early events in lymphocyte activation involve 3 different sets of proteins which are phosphorylated by CaM kinase, PKC and other kinases, and those kinases do not work sequentially, but rather, independently or cooperatively.

• Korean Journal of Food Science and Technology
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• v.42 no.3
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• pp.350-354
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• 2010

Laminaria japonica polysaccharides (LP) were prepared from L. japonica through hot water extraction, ultrafiltration and gel chromatography. In this study, we investigated the immunomodulating activity of LP (0.25-1 mg/mL) on the mitogen/alloantigen reactive proliferation and killing activity of the Balb/c mouse splenocytes. The LP directly induced the proliferation of splenocytes that was stimulated with mitogen or alloantigen in a dose-dependent manner. The killing activity of cytotoxic T lymphocytes (CTLs) and lymphokine activated killer cells (LAKs) were enhanced significantly in the LP treated cells. Also, the treatment of splenocytes with LP increased production of interleukin-2 (IL-2). These results suggest that polysaccharides from L. japonica show a substantial immunomodulating activity in mouse immune cells.