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- 검색키워드
- 주제어 : Interleukin-2 (검색결과 136 건)
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Ciprofloxacin이 임파구의 증식과 Interleukin-2 및 Soluble interleukin-2 receptor의 유리에 미치는 영향
Ciprofloxacin is one of the new fluoroquinolones which have a strong bactericidal activities and broad antibacterial spectrum. Due to the great potential for the clinical use of these drugs it is important to investigate any possible positive or negative side effects on the host defense system. We studied to verify the effects of ciprofloxacin on the incorporation of [³H]thymidine, production of interleukin-2 (IL-2), and release of soluble interleukin-2 receptors (IL-2R) in the cultures of phytohemagglutinin stimulated human peripheral lymphocytes for 5 days. After 3 days, After 3 days, [³H]thymidine incorporation was significantly increased in those groups below the 20 ug/ml of ciprofloxacin with dose dependent manner. At 80 ug/ml of ciprofloxacin, however, the [³H]thymidine incorporation was almost completely inhibited all the time. On the other hand, IL-2 assay in culture supernatants shows that ciprofloxacin strongly increase the production of IL-2. After 3 days, IL-2 activity in culture supernatants are 160.7, 93.3, 4.0, and 40.4 IU/ml at concentrations of ciprofloxacin 80, 20, 5, and 1.25 ug/ml respectively, and 2.3 IU/ml that does not contain drug, as measured by enzyme immunoassay. The effect was significant at clinically achievable concentrations (below 5 ug/ml). The release of IL-2R was not affected below the 20 ug/ml of ciprofloxacin, but significantly decreased at 80 ug/ml of ciprofloxacin. These data show that quinolones increased IL-2 synthesis by mononuclear leukocytes and it suggests that the potential usefulness of these antibiotics, not only as antimicrobial agents, but also as modulators of immune responses.
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Interleukin-2와 Anti-CD3 단클론항체에 의한 T세포 증식 상승효과에 대한 Protein tyrosine kinase와 Protein kinase C의 역할
Culture of human peripheral T lymphocytes with immobilized anti-CD3 mAb plus IL-2 resulted in a marked proliferation. Although a synergistic response of immobilized anti-CD3 and interleukin-2 (IL-2) has been reported, the mechanism of the celluar signal transduction through T cell receptor(TCR) and IL-2 receptor(IL-2R) remains unresolved. The process of the T ce11 activation involves a series of biochemical events which ultimately leads to lymphocyte proliferation. The CD3/TCR is known to activate two signal transduction pathways. The first one is the activation of a protein kinase C(PKC) and a rise in intracelluar calcium levels The second pathway operates through protein tyrosine kinases(PTKs). Stimulation of the IL-2R induces an increase tyrosine phosphorylation of several celluar proteins by PTKs. In the present study, I have used the selective PTK inhibitor(genistein) or chronic PMA treatment(depletion of intracelluar PKC activity), to investigate the role of PTK or PKC in synergistic proliferation signals delivered by TCR and IL-2R. Genistein(30pg/ml) completely blocked IL-2 induced T cell proliferation, and inhibited anti-CD3 mAb or IL-2/anti-CD3 mAb induced T cell proliferation(93%, 94% respectively). The chronic PMA treatment, which depletes intracelluar PKC activity, failed to inhibit the proliferative response of T cell stimulated with IL-2 alone. But the chronic PMA treatment inhibit the proliferative response of T cell stimulated by anti-CD3 or anti-CD3 mAb plus IL-2(68.6%, 49.1% repectively) These results demonstrate that proliferation of T cells triggered via IL-2R appears to be dependent on PTKs activity and independent of PKC invovement. PTKs and PKC activity may be important in TCR/CD3 signaling. But the TCR/CD3 and IL-2R are coupled to different signal transduction pathways responsible for the synergistic T cell proliferation.
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IL-2 및 Anti-CD3에 의한 T 세포의 IL-2 Rα 발현의 상승작용 기전
Culture of human peripheral T lymphocytes with immobilized anti-CD3 mAb plus IL-2 resulted in a marked proliferation and the enhancing IL-2Rα mRNA expression. The process of the T cell activation involves a series of biochemical events which ultimately lead to the proliferation and the IL-2Rα mRNA expression. Although the above results have been observed, the celluar signal mechanisms between the proliferative response and the IL-2Rα mRNA expression through T cell receptor and IL-2 receptor remains unresolved. In the present study, I used genistein (the selective PTK inhibitor) or chronic PMA treatment (depletion of intracelluar PKC activity), to investigate the role of PTK or PKC both in a synergistic proliferation and in the enhancing IL-2Rα mRNA expression by IL-2/anti-CD3. Genistein (30㎍/ml) completely blocked IL-2 or IL-2/anti-CD3 induced T cell proliferation, and inhibited anti-CD3 induced T cell proliferation (93.4%). But genistein downregulated the IL-2Rα mRNA expression by IL-2, anti-CD3 and IL-2/anti-CD3. The chronic Pk1A treatment failed to inhibit the proliferation and the IL-2Rα mRNA expression by IL-2. But PKC depleted T cells stimulated with anti-CD3 mAb showed the decrease of the proliferation (68.6%) and IL-2Rα mRNA expression. In activated with IL-2/anti-CD3, the proliferative response showed a half of reduction, but the IL-2Rα mRNA expression were not regulated. These results demonstrate that proliferative response to IL-2 appears to be dependent on PTKs activity and independent of PKC involvement, but the IL-2Rα mRNA expression may be required another signals. PTKs and PKC activity may be important in TCR/CD3 signaling. But IL-2/anti-CD3 are coupled up different signal transduction pathways responsible for the synergistic T cell proliferation and the enhancing IL-2Rα mRNA expression.
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