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Kafe 바로가기주관연구기관 | 성균관대학교 SungKyunKwan University |
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연구책임자 | 이명식 |
참여연구자 | 이복률 |
보고서유형 | 2단계보고서 |
발행국가 | 대한민국 |
언어 | 한국어 |
발행년월 | 2013-07 |
과제시작연도 | 2012 |
주관부처 | 미래창조과학부 Ministry of Science, ICT and Future Planning |
등록번호 | TRKO202100004805 |
과제고유번호 | 1345176108 |
사업명 | 바이오·의료기술개발 |
DB 구축일자 | 2021-07-10 |
키워드 | 선천면역.대식세포.관용.유사 Toll 수용체.염증.innate immunity.macrophages.tolerance.TLR.inflammation. |
Ⅳ. 연구개발결과
TLR2 tolerance와 DPP4 inhibition의 병합으로 기존에 1형 당뇨병을 발생전 억제하는 것에서 일보 전진하여 이미 발생한 1형 당뇨병을 치료하는데 성공. Non-TLR ligand는 in vitro에서는 작용하나 in vivo에서는 작용하지 않음을 관찰. HFD 후 intestinal innate immunity가 변하여 systemic low-grade inflammation, insulin resistance가 오는 것을 관찰하였고 antibiotics 치료하여 이를 reverse하여 새
Ⅳ. 연구개발결과
TLR2 tolerance와 DPP4 inhibition의 병합으로 기존에 1형 당뇨병을 발생전 억제하는 것에서 일보 전진하여 이미 발생한 1형 당뇨병을 치료하는데 성공. Non-TLR ligand는 in vitro에서는 작용하나 in vivo에서는 작용하지 않음을 관찰. HFD 후 intestinal innate immunity가 변하여 systemic low-grade inflammation, insulin resistance가 오는 것을 관찰하였고 antibiotics 치료하여 이를 reverse하여 새로운 치료 model 정립함. Microglia의 polarization, tolerance 등 표현형을 관찰할 수 있는 in vitro 및 in vivo 모델을 확립하고 이를 이용하여 특정 유전자의 기능 및 신호전달경로를 연구하였으며, polarization pattern을 성공적으로 규명함.
(출처 : 요 약 문 4p)
Aims: 1) to investigate the role of death/survival of macrophages, the most important cells in the innate immune system and its mechanism, 2) to explore the method of induction of TLR tolerance and its mechanism, and 3) to find the practical ways to apply those findings to disease models. Using thes
Aims: 1) to investigate the role of death/survival of macrophages, the most important cells in the innate immune system and its mechanism, 2) to explore the method of induction of TLR tolerance and its mechanism, and 3) to find the practical ways to apply those findings to disease models. Using these approaches, we may be able to find novel methods of controling innate immunity which can be applied to diverse inflammatory/immune disorders and apparently non-immune disorders where inflammation may play an important role.
Content: The phenomenon of TLR tolerance that occurs after repeated TLR stimulation is well known, however, the intracellular mechanism and its applicability to human disorders are not clearly elucidated. We studied the optimal method to induce macropahge tolerance by non-TLR ligands and its mechanism, which was employed to inhibit the development of autoimmune diabetes where TLR2 has been reported to play a critical role in the initiation of autoimmunity and sensitization of diabetogenic naive T cells. Such macrophage tolerance by non-TLR ligands was employed to treat established autoimmune diabetes in conjuction with methods to enhance decreased b-cell mass such as islet transplantation. Furthermore, we used another method of increasing b-cell mass - DPP4 inhibition, since the supply of islets is insufficient in clinical practice. Thus, we succeeded in the treatment of establihsed type 1 diabetes of NOD mice by induction of TLR tolerization in conjunction with DPP4 inhibition or islet transplantation. We also investigated the significance and mechanism of macrophage death, which was observed in apparently non-immune diseases such as obesity, type 2 diabetes or atherosclerosis. Finally, we studied the role of microglial cells, macrophages of the CNS, employing the same strategies described above to study the significance of micriglial cell function and viability in CNS disorders.
Implication & future application: Employing these methods aiming at innate immunity and macrophages, we found practical ways to prevent or treat autoimmune diseases such as autoimmune diabetes in conjunction with methods to replenish diminished islet b-cell mass such as islet transplantation. We elucidated the role of macrophage death in apparently non-immune disorders such as obesity, type 2 diabetes or atherosclerosis and its mechanism, which may be able to be applied to a wide spectrum of human diseases such as metabolic syndrome. These results will be applied to the development of clinically feasible methods for the treatment of established type 1 diabetes, type 2 diabetes associated with low-grade systemic inflammation or other neurological disorders characterized by inflammation.
(출처 : SUMMARY 5p)
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