연구성과물검색
유형별/분류별 연구성과물 검색
HOME ICON HOME > Search by Achievements Type > Reports View

Reports Detailed Information

https://www.krm.or.kr/krmts/link.html?dbGubun=SD&m201_id=10011564&local_id=10013419
FcRgIII에 의한 NKT 세포의 활성화가 자가 항체에 의해 유도되는 관절염에 미치는 영향 연구
Reports NRF is supported by Research Projects( FcRgIII에 의한 NKT 세포의 활성화가 자가 항체에 의해 유도되는 관절염에 미치는 영향 연구 | 2005 Year 신청요강 다운로드 PDF다운로드 | 김혜영(서울대학교(연건캠퍼스)) ) data is submitted to the NRF Project Results
Researcher who has been awarded a research grant by Humanities and Social Studies Support Program of NRF has to submit an end product within 6 months(* depend on the form of business)
  • Researchers have entered the information directly to the NRF of Korea research support system
Project Number E00012
Year(selected) 2005 Year
the present condition of Project 종료
State of proposition 재단승인
Completion Date 2006년 10월 20일
Year type 결과보고
Year(final report) 2006년
Research result report
  • Abstract
  • NKT cells promote antibody-induced arthritis, but the mechanism by which NKT cells are activated in this model remains unclear. It has been proposed that Fcgamma receptor (FcgammaR) contributes to NKT cell activation in antibody-induced arthritis. To address this issue, we explored the functions of FcgammaR on NKT cells in antibody-induced arthritis. RT-PCR and flow cytometric analysis demonstrated that NKT cells constitutively express surface FcgammaRIII but not FcgammaRI, -II, or -IV. FcgammaRIII engagement by aggregated IgG on NKT cells enhanced CD25 and CD69 expression, whereas FcgammaR(-/-) mouse NKT cells did not enhance activation. FcgammaRIII engagement on NKT cells enhanced the production of IL-4, IL-10, IL-13, and IFN-gamma, whereas FcgammaR-deficient NKT cells did not alter the production of these cytokines after aggregated IgG treatment. However, FcgammaR-deficient NKT cells were functionally intact in terms of TCR-induced activation. Moreover, adoptive transfer of FcgammaR-deficient NKT cells could not restore inflammation or TGF-beta production in the joint tissues of CD1d(-/-) mice, whereas adoptive transfer of wild-type NKT cells induced arthritis and reduced TGF-beta production in joint tissues. We conclude that FcgammaRIII engagement by IgG in joint tissues provides activating signals to NKT cells in antibody-induced arthritis.
  • Research result and Utilization method
  • 이전 연구를 통해, 자가항체에 의한 관절에서 NKT 세포가 중요한 역할을 담당하고 있다는 것을 확인하였다.
    본 연구에서는 NKT 세포가 관절염을 유도하는데 어떠한 기전이 관여되는지에 대해 확인하였다.
    NKT 세포는 TCR를 통한 신호가 전달되었을 때 활성화되는 것으로 많이 알려져있었다.
    이번 실험결과, TCR를 통한 신호뿐만아니라, FcR를 통한 신호도 NKT세포를 활성화 시키는데 중요한 것으로 확인되었으며, 관절염과 같은 자가면역질환에 관여하는 자가항체들이 NKT 세포를 활성화 시킴으로서 질병을 악화시킬 수 있다는 사실을 확인할 수 있었다.
  • Index terms
  • FcR, NKT, cytokine, arthritis
  • List of digital content of this reports
데이터를 로딩중 입니다.
  • This document, it is necessary to display the original author and you do not have permission
    to use copyrighted material for-profit
  • In addition , it does not allow the change or secondary writings of work
데이터 이용 만족도
자료이용후 의견
입력