• BMB Reports
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• v.55 no.2
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• pp.57-64
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• 2022

Autoimmune disease is known to be caused by unregulated self-antigen-specific T cells, causing tissue damage. Although antigen specificity is an important mechanism of the adaptive immune system, antigen non-related T cells have been found in the inflamed tissues in various conditions. Bystander T cell activation refers to the activation of T cells without antigen recognition. During an immune response to a pathogen, bystander activation of self-reactive T cells via inflammatory mediators such as cytokines can trigger autoimmune diseases. Other antigen-specific T cells can also be bystander-activated to induce innate immune response resulting in autoimmune disease pathogenesis along with self-antigen-specific T cells. In this review, we summarize previous studies investigating bystander activation of various T cell types (NKT, γδ T cells, MAIT cells, conventional CD4⁺, and CD8⁺ T cells) and discuss the role of innate-like T cell response in autoimmune diseases. In addition, we also review previous findings of bystander T cell function in infection and cancer. A better understanding of bystander-activated T cells versus antigen-stimulated T cells provides a novel insight to control autoimmune disease pathogenesis.

• IMMUNE NETWORK
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• v.12 no.6
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• pp.230-239
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• 2012

Activation-induced cytidine deaminase (AID) is an enzyme that is predominantly expressed in germinal center B cells and plays a pivotal role in immunoglobulin class switch recombination and somatic hypermutation for antibody (Ab) maturation. These two genetic processes endow Abs with protective functions against a multitude of antigens (pathogens) during humoral immune responses. In B cells, AID expression is regulated at the level of either transcriptional activation on AID gene loci or post-transcriptional suppression of AID mRNA. Furthermore, AID stabilization and targeting are determined by post-translational modifications and interactions with other cellular/nuclear factors. On the other hand, aberrant expression of AID causes B cell leukemias and lymphomas, including Burkitt's lymphoma caused by c-myc/IgH translocation. AID is also ectopically expressed in T cells and non-immune cells, and triggers point mutations in relevant DNA loci, resulting in tumorigenesis. Here, I review the recent literatures on the function of AID, regulation of AID expression, stability and targeting in B cells, and AID-related tumor formation.

• Proceedings of the Plant Resources Society of Korea Conference
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• 2020.08a
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• pp.87-87
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• 2020

In this study, we investigated the immune-enhancing activity of water extracts from Hydrangea macrophylla subsp. serrata (WE-HML). WE-HML increased cell viability and production of immunomodulators, which contributed to activating phagocytic activity in RAW264.7 cells. Inhibition of JNK and NF-κB reduced the production of immunomodulators by WE-HML. ROS inhibition suppressed the production of immunomodulators, and the activation of JNK and NF-κB signaling by WE-HML. TLR4 inhibition attenuated the production of immunomodulators, and activation of JNK and NF-κB signaling by WE-HML. In the immunosuppressed mouse model, WE-HML increased the spleen index, the levels of the cytokines, the numbers of white blood cells, lymphocytes, and neutrophils. However, WE-HML inhibited LPS-mediated overproduction of pro-inflammatory mediators in RAW264.7 cells, which indicated that WE-HML may have anti-inflammatory activity under excessive inflammatory conditions. Taken together, WE-HML may be considered to have immune-enhancing activity and expected to be used as a potential immune-enhancing agent.

• IMMUNE NETWORK
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• v.9 no.4
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• pp.115-121
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• 2009

Natural killer (NK) cells play key roles in innate and adaptive immune defenses. NK cell responses are mediated by two major mechanisms: the direct cytolysis of target cells, and immune regulation by production of various cytokines. Many previous reports show that the complex NK cell activation process requires de novo gene expression regulated at both transcriptional and post-transcriptional levels. Specialized un-translated regions (UTR) of mRNAs are the main mechanisms of post-transcriptional regulation. Analysis of posttranscriptional regulation is needed to clearly understand NK cell biology and, furthermore, harness the power of NK cells for therapeutic aims. This review summarizes the current understanding of mRNA metabolism during NK cell activation, focusing primarily on post-transcriptional regulation.

• Journal of Life Science
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• v.10 no.4
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• pp.362-364
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• 2000

Opuntia ficus-indca(Op) extract has been claimed to have several therapeutic properties in oriental medicine including anti-inflammatory and anti-rheumatoid arthritis effects. Little is known of its effect on the activation of immune cells such as T cells and macrophages. To evaluate the functional effect of Op extract on immune cells, we examined whether Op extract stimulates the proliferation of T cells and the secretion of cytokines including IL-1 beta, IL-6 and tumor necrosis factor-alpha in THP-1 cell lines by RT-PCR. Op extract significantly enhanced the proliferation of T cell clone(D10S). Transcription of cytokines including IL-1 beta, IL-6, and TNF-alpha peaked 6 hrs after exposure to Op extract(100g/ml) in the THP-1 cell line and declined and declined thereafter. In an experiment to test the dose dependency of transcription of cytokines, transcription increased at a dose of 10 g/ml and the maximum expression was obtained at 100 g/ml, 6 hrs after exposure to Op extract. These findings suggest that Op extract is a potent stimulant of immune cells including T cells and macrophages, which acts by stimulating T cell proliferation and upregulating cytokines. These phenomena imply that some edible plants may be beneficial to living animals through the activation of immune functions.

• Advances in Traditional Medicine
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• v.4 no.3
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• pp.163-170
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• 2004

The effect of immune activation by Echinacea purpurea was investigated by measuring total immunoglobulin (Ig) G, IgM. and the radioprotective effect of immune activation by Echinacea purpurea was investigated by measuring T lymphocyte subsets in the peripheral blood of mice following whole body irradiation. Echinacea purpurea activated macrophages to stimulate $IFN-{\gamma}$ production in association with the secondary activation of T lymphocytes, resulting in a decrease in IgG and IgM production. Cytokines released from macrophages in mouse peripheral blood after Echinacea purpurea administration activated helper T cells to proliferate. In addition, activated macrophages in association with the secondary T lymphocyte activation increased $IFN-{\gamma}$ production and stimulated proliferation of cytotoxic T cells and suppressor T cells, indicating the activation of cell-mediated immune responses.

• BMB Reports
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• v.55 no.10
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• pp.473-480
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• 2022

Neutrophils, the most abundant innate immune cells, play essential roles in the innate immune system. As key innate immune cells, neutrophils detect intrusion of pathogens and initiate immune cascades with their functions; swarming (arresting), cytokine production, degranulation, phagocytosis, and projection of neutrophil extracellular trap. Because of their short lifespan and consumption during immune response, neutrophils need to be generated consistently, and generation of newborn neutrophils (granulopoiesis) should fulfill the environmental/systemic demands for training in cases of infection. Accumulating evidence suggests that neutrophils also play important roles in the regulation of adaptive immunity. Neutrophil-mediated immune responses end with apoptosis of the cells, and proper phagocytosis of the apoptotic body (efferocytosis) is crucial for initial and post resolution by producing tolerogenic innate/adaptive immune cells. However, inflammatory cues can impair these cascades, resulting in systemic immune activation; necrotic/pyroptotic neutrophil bodies can aggravate the excessive inflammation, increasing inflammatory macrophage and dendritic cell activation and subsequent T_H1/T_H17 responses contributing to the regulation of the pathogenesis of autoimmune disease. In this review, we briefly introduce recent studies of neutrophil function as players of immune response.

• Journal of Life Science
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• v.18 no.6
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• pp.891-896
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• 2008

The function of mast cells as effector cells in allergy has been extensively studied. Mast cells activated through high affinity IgE-receptor ($Fc{\varepsilon}RI$) release diverse mediators, and lead to smooth muscle constriction, vasodilation, increase of vascular permeability, leukocyte recruitment and activation, mucus secretion, and tissue proliferation and remodeling. However, various other immunological and non-immunological signals can lead to the activation of mast cells. In resent years, mast cells have been identified to be involved in a complex range of immune functions. Mast cells can be important as key players in the regulation of innate as well as adapted immune responses, and may influence the development of allergy, autoimmune disorder and peripheral tolerance. This review summarizes the recent advances in the understanding of effector functions of mast cells in immune responses.

• Biomedical Science Letters
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• v.29 no.4
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• pp.376-381
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• 2023

Abscopal effect is a form of secondary immune response that occurs in ionizing radiation therapy, resulting in changes in the immune response through activation of immune cells such as macrophages and T lymphocytes. UVB causes DNA damage similar to ionizing radiation and causes similar intracellular reactions, so it is often used as an alternative in research on the effects of ionizing radiation. In a previous study, we found that pro-inflammatory cytokines, including TNF-α, increased in Jurkat T cells exposed to TGs. In this study, we confirmed the effects of UVB irradiation on T lymphocytes exposed to TGs, similar to the effects of ionizing radiation. As a result, it was shown that the mRNA expression of pro-inflammatory cytokines such as IL-1β and IFN-γ in Jurkat T cells exposed to TGs increased by UVB irradiation. In addition, it was confirmed that the increase in the expression of pro-inflammatory cytokines caused by UVB was caused by the activation of iNOS protein. This is very similar to the immune response that occurs when T lymphocytes are exposed to TGs. These results suggest that activation of iNOS protein is involved in the increase in pro-inflammatory cytokines caused by UVB irradiation in T lymphocytes exposed to TGs.

• Journal of Life Science
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• v.33 no.3
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• pp.295-303
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• 2023

Immune and metabolic systems are important factors in maintaining homeostasis. Immune response and metabolic regulation are highly associated, so, when the normal metabolism is disturbed, the immune response changed followed the metabolic diseases occur. Likewise, obesity is highly related to immune response. Obesity, which is caused by an imbalance in energy metabolism, is associated with metabolic diseases, such as insulin resistance, type 2 diabetes, fatty liver diseases, atherosclerosis and hypertension. As known, obesity is characterized in chronic low-grade inflammation. In obesity, the microenvironment of immune cells became inflammatory by the unique activation phenotypes of immune cells such as macrophage, natural killer cell, T cell. Also, the immune cells interact each other in cellular or cytokine mechanisms, which intensify the obesity-induced inflammatory response. This phenomenon suggests the possibility of regulating the activation of immune cells as a pharmacological therapeutic strategy for obesity in addition to the common pharmacological treatment of obesity which is aimed at inhibiting enzymes such as pancreatic lipase and α-amylase or inhibiting differentiation of preadipocytes. In this review, we summarize the activation phenotypes of macrophage, natural killer cell and T cell, and their aspects in obesity. We also summarize the pharmacological substances that alleviates obesity by regulating the activation of immune cells.