• 제목/요약/키워드: interleukin-2 (IL-2)

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Conjugated Linoleic Acid(CLA)의 암세포 증식 억제효과 및 Interleukin-1과 Interleukin-2의 생성에 미치는 영향 (Effects of Conjugated Linoleic acid(CLA) on the Growth of Tumor Cells and the Production of Interleukin-1 and Interleukin-2)

  • 김소희;김광혁;박건영
    • 한국식품영양과학회지
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    • 제26권5호
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    • pp.972-977
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    • 1997
  • Conjugated dienoic derivatives of linoleic acid(CLA) are a series of positional and gemotric isomers of linoleic acid which are found naturally in food, mainly dietary products and breef. We studied the effects of CLA on the growth of tumor cells and the production of interleukin-1(IL-1) and interleukin-2(IL-2). CLA treatment markedly inhibited the growth of Yac-1 cells and sarcoma-180 cells by 99 and 82% to that of control, respectively, after four days of incubation at 37$^{\circ}C$. To elucidate the immunological mechanism of antitumor activity of CLA, spleen cells of Balb/c mouse were exposed to 31, 63, 125, 250 $\mu\textrm{g}$ of CLA per ml for 24 hrs at 37$^{\circ}C$. The culture supernatants of CLA-exposed spleen cells reduced the production of IL-1 and IL-2 in all of the test conditions. These results indicate that the anticarcino-genic effect of CLA was mediated by the other actions rather than the production of the Il-1 or IL-2. We suggest that CLA might have an antiinflammatory effect in part due to its inhibitory action on the production of IL-1.

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($17{\beta}$-Estradiol 및 1,25-Dihydroxyvitamin $D_3$가 치주인대 세포의 Interleukin-6의 생성에 미치는 영향 (Effect of $17{\beta}$-Estradiol and 1,25-Dihydroxyvitamin $D_3$ on Interleukin-6 Production of Periodontal Ligament Cells)

  • 곽월아;최봉규;이현정;유윤정
    • Journal of Periodontal and Implant Science
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    • 제29권3호
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    • pp.645-654
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    • 1999
  • Interleukin-6(IL-6) stimulate osteoclast differentiation. $17{\beta}$-estradiol, 1,25-dihydroxyvitamin $D_3$(1,25-$(OH)_2D_3$) and interleukin-$1{\beta}$ inhibit or stimulate osteoclast differentiation by decreasing or increasing the synthesis of interleukin-6(IL-6) from stromal/osteoblastic cells, respectively. Periodontal ligament(PDL) cells reside between the alveolar bone and the cementum and have osteoblastic characteristics. To estimate the effect of $17{\beta}$-estradiol and 1,25$(OH)_2D_3$ on IL-6 production of PDL cells, PDL cells were treated with $17{\beta}$-estradiol or 1,25-$(OH)_2D_3$ in the absence or the presence of IL-$1{\beta}$. The concentration of IL-6 produced form PDL cells was determined by enzym linked immunosorbent assay(ELISA). In unstimulated PDL cells, we detected constitutive production of IL-6 at 1st and 2nd day. IL-$1{\beta}$ increased IL-6 synthesis at 1st day and 2nd day. $17{\beta}$-estradiol had no significant effect on the secretion of this cytokine, either constitutively or after stimulation with IL- $1{\beta}$(0.05 ng/ml). 1,25-$(OH)_2D_3$($10^{-8}M$) decreased not only constitutive IL-6 production but also IL-$1{\beta}$-induced IL-6 production at 2nd day. These results suggest that 1,25-$(OH)_2D_3$ may control IL-$1{\beta}$-induced osteoclast differentiation by decreasing IL-$1{\beta}$-induced IL-6 secretion of PDL cells.

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마우스에 있어서 Interleukin -2의 투여방법이 Meth-A 종양세포에 대한 항암효과에 미치는 영향 (Effect of Interleukin-2 Administration Route on Antitumor Response Against Subcutaneous Meth-A Tumor in Mice)

  • 권오덕
    • 한국임상수의학회지
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    • 제17권2호
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    • pp.311-315
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    • 2000
  • Recombinant interleukin-2 (IL-2) has been demonstated as an antineoplastic agent in mice and human, and the route of administration is important to IL-2-induced therapeutic responses. Therefore, the current experiment was undertaken to clarify the effect of IL-2 administration route on antitumor response against subcutaneous Meth-A tumor in mice. At the beginning of each experiment, normal BALB/c mice were injected subcutaneously with $5{\times}10^6$ Meth-A tumor cells. Beginning on day 7, experimental groups were treated with a 5-day course of IL-2 (intraperitoneal or subcutaneous injection of 30, 000 IU every 12 hours for 5 days). The result of this experiment revealed that Meth-A tumor grew progressively in control mice. Intraperitoneal IL-2 treatment decreased significantly tumor growth and prolonged survival, compared with control mice. Subcutaneous IL-2 treatment decreased significantly tumor growth until day 11 and tumor cells, grew progressively thereafter, but mice in this group survived longer than control mice.

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Interleukin-18 Synergism with Interleukin-2 in Cytotoxicity and NKG2D Expression of Human Natural Killer Cells

  • Qi, Yuan-Ying;Lu, Chao;Ju, Ying;Wang, Zi-E;Li, Yuan-Tang;Shen, Ya-Juan;Lu, Zhi-Ming
    • Asian Pacific Journal of Cancer Prevention
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    • 제15권18호
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    • pp.7857-7861
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    • 2014
  • Natural killer (NK) cells play an important role in anti-tumor immunity. Interleukin (IL)-18 is an immunoregulatory cytokine that induces potent NK cell-dependent anti-tumor responses when administrated with other cytokines. In this study, we explored the effects of combining IL-18 and IL-2 on NK cytotoxicity as well as expression levels of the NK cell receptor NKG2D in vitro. Freshly isolated PBMCs were incubated for 48 h with IL-18 and IL-2, then CD107a expression on $CD3^-CD56^+$ NK cells was determined by three-colour flow cytometry to evaluate the cytotoxicity of NK cells against human erythroleukemia K562 cells and human colon carcinoma HT29 cells. Flow cytometric analysis was also employed to determine NKG2D expression on NK cells. The combined use of IL-18 and IL-2 significantly increased CD107a expression on NK cells compared with using IL-18 or IL-2 alone, suggesting that the combination of these two cytokines exerted synergistic enhancement of NK cytotoxicity. IL-18 also enhanced NKG2D expression on NK cells when administered with IL-2. In addition, blockade of NKG2D signaling with NKG2D-blocking antibody attenuated the up-regulatory effect of combining IL-18 and IL-2 on NK cytolysis. Our data revealed that IL-18 synergized with IL-2 to dramatically enhance the cytolytic activity of human NK cells in a NKG2D-dependent manner. The results appear encouraging for the use of combined IL-18 and IL-2 in tumor immunotherapy.

온도 및 염분 등의 환경요인이 참돔(Pagrus major)의 Interleukin-1 Receptor Accessory Protein 발현에 미치는 영향 (Effects of Environmental Factors Such as Temperature and Salinity on Expression of Interleukin-1 Receptor Accessory Protein in the Red Seabream (Pagrus major))

  • 강한승;민병화
    • 한국해양생명과학회지
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    • 제2권2호
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    • pp.70-74
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    • 2017
  • IL-1RAcP는 일명 interleukin-1 receptor accessory protein이라 칭하며 interleukin-1 염증성 사이토카인과 interleukin-1 receptor I (IL-1RI) 결합체와 복합체를 형성하여 작용한다. IL-1RAcP는 면역반응, 스트레스 및 세포사멸과 관련이 있다. 본 연구의 목적은 참돔(Pagrus major)을 저수온(8℃, 33 psu) 및 저염분(20℃, 10 psu) 상태에 노출시킨 후, IL-1RAcP 유전자의 발현을 관찰하는 것이다. 연구결과, IL-1RAcP 유전자의 발현은 저수온(8℃, 33 psu) 및 저염분(20℃, 10 psu) 상태에서 유의적으로 증가하는 것으로 나타났다. 이 연구결과로서 IL-1RAcP 유전자는 저수온 및 저염분 등의 환경 스트레스에 대한 생체지표유전자로서 역할을 한다고 제의한다.

정신분열증 환자에서 Interleukin-$1{\beta}$, -2, -6 생산능과 혈청농도 변화에 관한 연구 (Study on Alteration of Interleukin-$1{\beta}$, -2, -6 Production and Serum Level in Schizophrenic Patients)

  • 김용구;이민수;서광윤
    • 생물정신의학
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    • 제1권1호
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    • pp.98-108
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    • 1994
  • The etiology and pathophysiology of schizophrenia remain unknown. It has been postulated that infectious-autoimmune process may play a role in the pathogenesis of symptoms in some schizophrenic patients. Findings of altered interleukin(IL) regulation have been regarded as additional proof that schzophrenia has an infectious-autoimmune background. In the present study, we measured mitogen-stimulated production of and serum level of IL-$1{\beta}$, IL-2, IL-6 using ELISA in 16 neuroleptic-free schizophrenic patients and in 16 age, sex matched healthy controls. The results were as follows : 1) There was a significant decrease of IL-2 production in schizophrenic patients than in normal controls(respectively $1.90{\pm}0.13ng/m{\ell}$, $2.79{\pm}0.14ng/m{\ell}$, p<0.001). But there was no significant difference of IL-$1{\beta}$ production and IL-6 production between schizophrenic patients and normal controls. 2) There was a significant increase of serum level of IL-2 in schizophrenic pateitns than in normal controls(respectively $184.8{\pm}12.8pg/m{\ell}$, $104.2{\pm}34.2pg/m{\ell}$, p<0.01). Serum level of IL-$1{\beta}$ was partially detected in both groups and serum level of IL-6 was not detected in both groups. 3) There was no significant differences of IL-$1{\beta}$, -2, -6 production & serum level of IL-2 according to male vs female, paranoid type vs undifferentiated type, drug-naive group vs drug-free group in schizophrenic patients. 4) There was significant correlation between IL-$1{\beta}$ and IL-6 production(r=0.86, p<0.001). No correlation between IL-$1{\beta}$, -2, -6 production, serum level of IL-2 and age, duration of illness, and BPRS score was found. It has been suggested that the low lymphocyte production of IL-2 in the patients with autoimmune disease occurs because the T cells are activated and lymphocyte-derived IL-2 has been released into the serum. The authors suggest that decreased IL-2 production in our schizophrenic patients is due to increased IL-2 serum level in those patients. Thus our finding of low IL-2 production and high serum level of IL-2 in our schizophrenic patients is compatible with the possibility that our patients have an autoimmune process. Further study on relationship between IL alteration and other immunological abnormalities(the presence of serum autoantibody and of anti-brain antibody, $CD4^+$, $CD8^+$ cell index, etc) in schizophrenic patients will be warranted.

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마우스에서 Interleukin-2가 RD-995 종양세포에 미치는 항암효과 (Effect of interleukin-2 on antitumor response against intraperitoneal RD-995 tumor in mice)

  • 권오덕
    • 한국동물위생학회지
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    • 제25권3호
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    • pp.309-314
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    • 2002
  • Recombinant interleukin-2(IL-2) has demonstrated as an antineoplastic agent in mice and human, but the relatively low response rates observed in clinical trials. Therefore, the present study was undertaken in order to evaluate therapeutic activities of IL-2 for the establishment of therapeutic applications. At the onset of the experiment, normal C3H/HeN mice were injected with 5$\times$10$\^$6/ RD-995 tumor cells, murine ultraviolet radiation-induced fibrosarcoma, intraperitoneally. Beginning on day 6, experimental groups were treated with a 5-day course of IL-2(subcutaneous injection of 30,000 IU every 12 hours for 5 days). The result of this experiment revealed that body weight gradually decreased from 20th day in control mice. Subcutaneous IL-2 therapy prevented partially decrease body weight, and prolonged survival of mice compared with control group.

마우스에서 자외선 조사에 의해 유도된 종양세포에 대한 Interleukin-2의 항암효과 (Effect of Interleukin-2 on Antitumor Response Against Ultraviolet Radiation-Induced Fibrosarcoma in Mice)

  • 권오덕
    • 한국임상수의학회지
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    • 제18권1호
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    • pp.14-17
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    • 2001
  • Recombinant interleukin-2 (IL-2) has demonstrated as an antineoplastic agent in mice and human, but the relatively low response rates observed in clinical trials. Therefore, the present study was undertaken in order to evaluate therapeutic activities of IL-2 for the establishment of therapeutic applications. At the onset of the experiment, normal C3H/HeN mice were injected with $3{\times}10^6$ RD-995 tumor cells, murine ultraviolet radiation-induced fibrosarcoma, subcutaneously. Beginning on day 25, experimental groups were treated with a 5-day course of IL-2 (subcutaneous injection of 30,000 IU every 12 hours for 5 days). The result of this experiment revealed that RD-995 tumor grew progressively in control mice. Subcutaneous IL-2 therapy decreased tumor growth until day 23, then the tumor grew progressively. No significant difference in the survival of IL-2 therapy decreased tumor growth until day 23, then the tumor grew progressively. No significant difference in the survival of IL-2 therapy decreased tumor growth until day 23, then the tumor grew progressively. No significant difference in the survival of IL-2 treated mice were observed compared with the control mice.

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RAW 264.7 cell의 염증반응에 대한 산열음자(散熱飮子)의 항염증 효과 (Effect of Sanyeoleumja on Inflammatory Response of RAW 264.7 Cells)

  • 김태연
    • 동의생리병리학회지
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    • 제34권1호
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    • pp.7-13
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    • 2020
  • Sanyeoleumja (SY) is the traditional Korean medicinal prescription for the treatment of inflammatory diseases of eyes. In this study, the anti-inflammatory effects of SY water extract were investigated. To measure the anti-inflammatory effects of SY, we examined the productions of inflammatory factor including nitric oxide (NO), prostaglandin E2 (PGE2), inducible nitric oxide synthase (iNOS), cyclooxygenase-2 (COX-2), interleukin-6 (IL-6), interleukin-1β (IL-1β) in lipopolysaccharide (LPS)-induced RAW 264.7 cells. SY inhibited NO and PGE2 production in a dose dependent manner and decreased the protein and mRNA expression of iNOS and COX-2. Also, SY decreased the mRNA expression of interleukin-6 (IL-6) and interleukin-1β (IL-1β). In conclusion, SY downregulated LPS-induced inflammatory factor productions, which could be a clinical basis for inflammatory diseases.

Suppression of Interleukin-2 Expression by Arachidonylethanolamide is Mediated by Down-regulation of NF-AT

  • Lee, Jung-Hee;Park, Kyung-Ran;Yea, Sung-Su
    • Molecular & Cellular Toxicology
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    • 제2권4호
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    • pp.223-228
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    • 2006
  • Several plant-derived cannabinoids and endogenous ligands for cannabinoid receptors such as 2-arachidonyl-glycerol have been known to inhibit interleukin-2 (IL-2) expression. In the present study, we utilized arachidonylethanolamide (AEA), a putative endogenous ligand for cannabinoid receptors, to determine whether AEA modulated the expression of IL-2. AEA inhibited phorbol 12-myristate 13-acetate (PMA) plus ionomycin (Io)-induced IL-2 protein secretion and mRNA expression in EL-4 mouse T-cells as determined by ELISA and RT-PCR, respectively. To further characterize the inhibitory mechanism of AEA at the transcriptional level, we performed promoter study for IL-2 gene in PMA/Io-stimulated EL-4 cells. AEA decreased the transcriptional activity of the nuclear factor of activated T-cells (NF-AT) as well as the IL-2 promoter activity. These results suggest that AEA suppresses IL-2 expression and that the inhibition is mediated, at least in part, through the down-regulation of NF-AT.