• Journal of the korean veterinary medical association
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• v.25 no.10
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• pp.595-606
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• 1989

항원제시세포(APC)와 보조T세포 간의 협력작용에 의하여 활성화된 작동세포(NK세포, CTL, K세포, 대식세포, 과립구 등)의 종양세포, 이식장기 및 세포내기생세균에 감염된 각종 세포에 대한 세포독성작용은 생체방어를 위한 중요한 세포성면역기전이다. 지난 몇 년간 세포성면역기전에 관한 많은 연구에도 불구하고 T림파구매개성 세포독성작용의 면역생물학적기전은 확실히 밝혀있지 않다. 지금까지 알려진 중요한 연구내용을 요약하면 다음과 같다. 1. 세포독성작용을 나타내는 작동세포로는 NK세포, CTL, K세포, 대식세포/단핵구 및 과립구가 있다. 2. T세포의 세포표면항원분자군(CD)으로는 $CD_{2},\;CD_{3},\;CD_{4}[Ly_{3}T_{4}],\;CD_{5}[=Ly_{1}],\;CD_{7},\;CD_{8}[Ly_{2,3}]$가 있으며 $CD_{4}$는 보조Ttpvhdml 특이마커이고 $CD_{8}$는 세포독성 T세포 및 억압T세포의 특이마커이다. 주요 T세포수용체(TCR)는 $CD_{4}$ 또는 $CD_{8}$ 분자와 가까이 연합된 이향체($TCR-{\alpha}{\beta}/TCR-{\gamma}{\delta}$이며 보조 T세포 $CD_{4}$(마우스 $L_{3}T_{4}$)는 수용체와 연합되어 있는반면 억압 T세포 $CD_{8}(Ly+_{2,3})$는 항원수용체와 연합되어 있다. 3. T세포는 Ti-$CD_{3}$(항원/MHC) 복합체를 통한 '항원가교'에 의한 자극(항원인식)과 $CD_{2}$를 통한 비특이경로에 의하여 활성화(분화증식)된다. 비특이경로를 통한 활성경로에서 T세포($CD_{4}$ 및 $CD_{8}$)가 활성화되기 위하여는 보조T세포가 생산하는 IL-2을 요구하며 IL-2의 자극으로 분화증식된 $CD_{8}$는 세포독성능을 나타내지만 $CD_{4}^{+}$는 여전히 세포독성능을 나타내지 못한다. 4. 보조T세포는 class II MHC분자와 연합된 항원을 식별하는 반면 세포독성T세포는 class I MHC 분자와 연합된 항원을 식별한다. 5. 림파구 매개성 세포독성은 접촉(conjugati-on), 탈분극(depolarization), 용해계획(progra-mming), 용해(lysis) 및 재순환(recycling)의 단계를 거쳐 진행된다. 6. 표적세포살해매체로는 perforin / PFP / cy-tolysin, lymphopores, lymphotoxins, protone, cytolytic enzymes가 알려졌으며 세포독성작용은 이들 이외에도 여러 가지 매체를 통한 복합작용으로 추정된다. 7. CTL 매개성 표적세포의 주요 대사변화는 actomyocin ATPase의 증가, phosphocreatine과 ATPase의 소모, ATP 의존성 $Na^{+}/K^{+}$ 펌프작용의 중지, ATP 의존성 $Ca^{2+}$ 유출감소 및 세포내 축적이 관찰된다. 8. $Ca^{2+}$의 축적으로 세포막 교질 침투손상을 주어 수분의 유입을 증가시킴으로써 수포형성, 핵붕괴, 사립체팽화 및 정상세포 구조상실(Zeiosis)이 있다. 결론적으로 CTL 매개성 세포독성작용은 PFP, LT, TNF, 유사 TNF / LT 및 기타 매체를 통한 복합작용이며 세포살해기전은 지속적 대사소모와 정형적 세포구조(핵 및 세포질)의 파괴에 의한 것이다.

• Journal of the korean academy of Pediatric Dentistry
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• v.35 no.4
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• pp.597-606
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• 2008

Resorption of alveolar bone in periodontitis is due to excessive differentiation and activation of osteoclasts. Bacterial antigens causing periodontitis activates CD4 T cells, which leads to expressing RANK ligand (RANKL) on CD4 T cells. RANKL binds RANK on preosteoclasts or osteoclasts, and enhances the differentiation preosteoclasts into osteoclasts and the activation of mature osteoclasts. CD137, one of TNF receptor (TNFR) family, expressed on activated T cells binds with CD137 ligand (CD137L) on antigen presenting cells. Cross-linking of CD137 by CD137L acts as T cell co-stimulatory signals and, therefore, enhances the activation of T cell. In this study, I elucidated the biological responses of CD137L on (pre)osteoclasts and RANKL on T cells in the context of in vivo interaction between T cells and osteoclasts. RAW264.7, murine monocytic cells, constitutively express CD137L. Ligation of CD137L with anti-CD137L mAb inhibited RANKL-induced osteoclast formation in a dosedependent manner. Bone marrow cells are expressed CD137L by the treatment with M-CSF. Cross-linking of CD137L abolished M-CSF/ RANKL-evoked the formation of multi-nucleated osteoclasts. Both mouse CD4 and CD8 T cells are expressed RANKL following their activation. Ligation of RANKL with OPG, the decoy receptor for RANKL, inhibited both CD4 and CD8 T cell proliferation. These effects were attributed to RANKL-induced apoptosis. These data indicate that CD137L and RANKL on osteoclasts and T cells, respectively provide them with inhibitory signal.

• Journal of Life Science
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• v.31 no.9
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• pp.856-861
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• 2021

CD82/KAI1, identified as a metastasis suppressor, was initially known only as a molecular facilitator, but its various functions have recently been revealed. CD82 plays an important role in the stem-progenitor cell, angiogenesis, and muscle. We would like to introduce the recently reported functions and roles of CD82 in this review. CD82 is a member of the tetraspanin family, which consists of four transmembrane domains. The interaction between CD82 and cell adhesion molecules suppresses the metastasis of cancer. CD82 regulates the cell cycle of stem-progenitor cells in the stem cell niche. In the bone marrow, CD82 is expressed on long-term repopulating hematopoietic stem cells (LT-HSCs), which show multipotent differentiation potential. The interaction between CD82 and Duffy antigen receptor for chemokines (DARC) induces quiescence in LT-HSCs. CD82 also regulates Rac1 activity, resulting in the homing and engraftment of HSCs into the bone marrow niche. Besides, CD82 maintains the differentiation potential of muscle stem cells and prevents angiogenesis by inhibiting the expression of cytokines, such as IL-6 and VEGF and adhesion molecules in endothelial cells. CD82 is a key membrane protein that distinguishes the hierarchy of stem-progenitor cells, and is also important for amplification and verification of cellular resources. Further studies on the function of CD82 in various organs and cells are expected to advance cell biology and cell therapy.

• The Journal of Korean Society of Virology
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• v.26 no.2
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• pp.141-150
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• 1996

본 연구에서는 $CD4^+$ T 세포를 일회성으로 감염시킬 수 있고 $CD4^+$ T 세포에 HIV-1 envelope 유전자를 전달할 수 있는 바이러스 입자를 생산하는 HIV-1 complementation system을 개발하였고 이 system을 이용하여 $CD4^+$ T 세포에 선택적으로 HIV-1 envelope 당단백질을 발현시켰다. 이 system은 Gag/Gag-Pol expressor와 Env expressor로 구성되어있다. Gag/Gag-Pol expressor는 바이러스 입자 생산에 필요한 구조단백질과 기능단백질을 발현시키지만 packaging signal이 결핍되어 바이러스 입자로 유전자가 들어가지 못하도록 제조되었다. Env expressor는 Tat, Rev와 envelope 당단백질을 발현시키고 packaging signal을 갖고 있어 바이러스 입자로 envelope 유전자가 들어가도록 제조되었다. Gag/Gag-Pol expressor로부터 Gag와 Gag-Pol의 발현은 Rev 단백질을 요구하였고 Env expressor로부터 Rev 단백질 이 제공될 때 Gag와 Gag-Pol 단백질은 효율적으로 발현되었다. Gag/Gag-Pol과 Env expressor로 cotransfection된 COS-1 세포에서 $CD4^+$ T 세포를 일회성으로 감염시킬 수 있는 바이러스 입자가 생산되었다. 생산된 바이러스 입자는 $CD4^+$ T 세포에 HIV-1 envelope 유전자를 전달하여 envelope 당단백질을 발현시켰고 복제 가능한 자손 바이러스의 생성을 유도하지 못하였다. 본 연구에서 개발된 방법은 $CD4^+$ T 세포에서 envelope 당단백질의 기능을 분석하고 관심 있는 유전자를 $CD4^+$ T 세포에 전달하는 바이러스 입자의 생산에 이용할 수 있다.

• Journal of Life Science
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• v.19 no.12
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• pp.1690-1697
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• 2009

CD11c and costimulatory molecules such as CD80 and CD86 express mainly in dendritic cells (DCs). In this study, we investigated the biologic effects of recombinant Fms-like tyrosine kinase-3 (Flt-3) ligand on the expression of DC surface markers, including CD11c in leukemia cell lines, such as KG-1, HL-60, NB4, and THP-1 cells. The expression of the Flt-3 receptor was found in NB4 and HL-60 cells, as well as KG-1 cells, but not in THP-1 cells. When KG-1 cells were cultured in a medium containing Flt-3 ligand or granulocyte macrophage-colony stimulating factor (GM-CSF) plus tumor necrosis factor (TNF)-$\alpha$, cell proliferation was inhibited and the expression levels of CD11c, major histocompatibility complex (MHC)-I, and MHC-II were increased in the cells. Flt-3 ligand also increased the expression level of CD11c on HL-60 and NB4 cells, but not on THP-1 cells. In comparison with CD11c expression, the expression level of CD11b on KG-1 cells, but not on NB4 and HL-60 cells, was slightly increased by Flt-3 ligand. Flt-3 ligand induced phosphorylation of extracellular signal-regulated kinase-1/2 (ERK-1/2) and p38-mitogen-activated protein kinase (p38-MAPK) in KG-1 cells, and the up-regulation of CD11c expression by Flt-3 ligand in the cells was abrogated by PD98059, an inhibitor of MEK. The results suggest that Flt-3 ligand up-regulates DC surface markers on $CD34^+$ myelomonocytic KG-1 cells, as well as promyelocytic leukemia cells, and that the differentiation of the leukemia cells into DC-like cells by Flt-3 ligand is mediated by ERK-1/2 activity.

• Journal of the korean academy of Pediatric Dentistry
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• v.46 no.3
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• pp.337-342
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• 2019

The aim of this study was to analyze cells from human dental pulp tissue of impacted supernumerary teeth as stem cells with flow cytometry. Human dental pulp cells from 15 supernumerary teeth were identified their characteristics as stem cells by expression of mesenchymal stem cell markers through flow cytometry analysis at passage 3 and passage 10. Cluster of differentiation (CD) 73, CD 90, CD 34, CD 45 and STRO-1 cell surface markers were used to figure out characteristics of dental pulp stem cells from supernumerary teeth. At passage 3, the cell population showed positive expression of CD 73, CD90 and STRO-1, lacked expression of CD 34 and CD 45. At passage 10, CD 73, CD 90 and STRO-1 showed positive expression while CD 34 and CD 45 showed negative expression. This study indicated that dental pulp stem cells of supernumerary teeth had the properties of mesenchymal stem cells at both early and late passage. Impacted supernumerary teeth could be considered as a noble source of stem cells because of rapid growth and maintaining characteristics of stem cells until late passage.

• Journal of Ginseng Research
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• v.33 no.4
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• pp.324-329
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• 2009

Cell-cell adhesion managed by various adhesion molecules is known to be one of pathophysiological phenomena found in numerous immunological diseases such as rheumatoid arthritis and allergic diseases. In this study, we examined the regulatory role of ginsenosides (G)- Rh1, reported to display anti-inflammatory and anti-allergic effects, on CD29-mediated cell adhesion. G-Rh1 significantly suppressed U937 cell-cell adhesion mediated by CD29 but not CD43. It also blocked U937 cell-fibronectin adhesion, mediated by activated CD29, up to 30%. In agreement, this compound also significantly decreased the surface level of CD29 but not CD43 as well as other costimulatory molecules such as CD69, CD80, and CD86. Therefore, these results suggest that G-Rh1 may have inhibitory function on CD29-mediated cell adhesion events, probably contributing to its anti-inflammatory and anti-allergic activities.

• Journal of Life Science
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• v.25 no.6
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• pp.686-692
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• 2015

Cancer is subject to dynamic interactions between contrary immune reactions that drive both tumor growth and suppression. Forkhead box p3 positive T cells (Foxp3 positive T cells) might support tumor promotion, while CD8 positive T cells might protect the host. The present study examined the distributions of CD8- and Foxp3-positive T cells and CD8 positive T cells/ Foxp3 positive T cells ratio in skin squamous cell carcinoma (SCC) and its precancerous lesions; it also compared this with data for basal cell carcinoma (BCC). Iimmunohistochemical staining for CD8 and Foxp3 was conducted in 20 cases of SCC, Bowen's disease (BD), actinic keratosis (AK) and BCC. The BD and SCC cases exhibited significantly increased numbers of both CD8- and Foxp3-positive T cells in their advancing regions compared with the AK and BCC cases, and the BD cases exhibited significantly lower CD8 positive T cells / Foxp3 positive T cells ratio in these regions than did the AK and BCC cases. There was no significant difference in both T cells and the ratio between BD and SCC. The degree of both T cells infiltration differed between the advancing and central areas in SCC and BCC. Immune micro-environments differ between cutaneous squamous cell tumors and BCC and differ as well among tumor compartments.

• Journal of Chest Surgery
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• v.43 no.5
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• pp.499-505
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• 2010

Background: There have been several reports using animal experiments that CD1-restricted T-cells have a key role in tumor immunity. To address this issue, we studied the expression of markers for CD1c+ myeloid dendritic cells (DCs) isolated from peripheral blood in the clinical setting. Material and Method: A total of 24 patients with radiologically suspected or histologically confirmed lung cancer who underwent pulmonary resection were enrolled in this study. The patients were divided according to histology findings into three groups: primary adenocarcinoma of lung (PACL), primary squamous cell carcinoma of lung (PSqCL) and benign lung disease (BLD). We obtained 20 mL of peripheral venous blood from patients using heparin-coated syringes. Using flow-cytometry after labeling with monoclonal antibodies, data acquisition and analysis were done. Result: The ratio of CD1c+CD19- dendritic cells to CD1c+ dendritic cells were not significantly different between the three groups. CD40 (p=0.171), CD86 (p=0.037) and HLA-DR (p=0.036) were less expressed in the PACL than the BLD group. Expression of CD40 (p=0.319), CD86 (p=0.036) and HLA-DR (p=0.085) were less expressed in the PACL than the PSqCL group, but the differences were only significant for CD86. Expression of co-stimulatory markers was not different between the PSqCL and BLD groups. Expression of markers for activated DCs were dramatically lower in the PACL group than in groups with other histology (CD40 (p=0.005), CD86 (p=0.013) HLA-DR (p=0.004). Conclusion: These results suggest the possibility that CD1c+ myeloid DCs participate in control of the tumor immunity system and that low expression of markers results in lack of an immune response triggered by dendritic cells in adenocarcinoma of the lung.

• Clinical and Experimental Reproductive Medicine
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• v.35 no.2
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• pp.119-129
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• 2008

Objective: The purpose of this study was to quantify decidual $CD56^+$ and $CD16^+$ NK cell subtype population and to evaluate the correlation between decidual NK cell expression and peripheral $CD56^+$ NK cell expression in women with a history of recurrent abortion and increased peripheral NK cells. Methods: Twenty-nine women with recurrent abortion and elevated peripheral $CD56^+$ NK cell percentage who had chromosomally normal conceptus were included in this study. Thirty-two women with recurrent abortion who had chromosomally abnormal conceptus were used as controls. Distribution of $CD56^+$ and $CD16^+$ NK cells in decidual tissues including implantation sites was examined by immunohistochemical staining. The degree of immunohistochemical staining was interpreted by score and percentage. Results: There was a significant difference in decidual $CD56^+$ NK cell score ($43.6{\pm}24.5$ vs. $23.9{\pm}16.3$ P =0.001) and $CD56^+$ NK cell percentage ($42.1{\pm}11.7$ vs. $33.9{\pm}15.8$ P =0.027) between increased peripheral NK cell group and control group. However, there was no statistically significant difference in decidual $CD16^+$ NK cell score ($18.7{\pm}9.5$ vs. $13.2{\pm}39.4$ P =0.108) and $CD16^+$ NK cell percentage ($24.7{\pm}5.9$ vs. $23.4{\pm}11.7$ P =0.599). There was no significant correlation between decidual NK cell score and peripheral NK cell percentage in increase peripheral NK cell group (peripheral $CD56^+$ NK cell percentage vs. decidual $CD56^+$ NK cell score, r=-0.016, P =0.932, peripheral $CD16^+$ NK cell percentage vs. decidual $CD16^+$ NK cell score, r=0.008, P =0.968). Conclusion: This study shows that $CD56^+$ decidual NK cells are increased in decidua of women exhibiting a history of recurrent abortion with increased $CD56^+$ peripheral NK cell. There was no significant correlation between decidual and peripheral NK cell increment in increase peripheral NK cell group. This study suggests the possibility that decidual NK cells may play an important role in the immune mechanism of recurrent abortion.