지원사업
학술연구/단체지원/교육 등 연구자 활동을 지속하도록 DBpia가 지원하고 있어요.
커뮤니티
연구자들이 자신의 연구와 전문성을 널리 알리고, 새로운 협력의 기회를 만들 수 있는 네트워킹 공간이에요.
논문 기본 정보
- 자료유형
- 학술저널
- 저자정보
- 발행연도
- 2017.6
- 수록면
- 192 - 200 (9page)
이용수
초록· 키워드
오류제보하기
Japanese encephalitis (JE) is neuroinflammation characterized by uncontrolled infiltration of peripheral leukocytes into the central nervous system (CNS). We previously demonstrated exacerbation of JE following CD11c<SUP>hi</SUP> dendritic cell (DC) ablation in CD11c-DTR transgenic mice. Moreover, CD11c<SUP>hi</SUP> DC ablation led to abnormal differentiation of CD11b<SUP>+</SUP>Ly-6C<SUP>hi</SUP> monocytes and enhanced permeability of the blood-brain barrier (BBB), resulting in promoting the progression of JE. Here, we examined changes in lymphoid and myeloid-derived leukocyte subpopulations associated with pro- and anti-inflammation during JE progression. The analyses of this study focused on regulatory CD4<SUP>+</SUP>Foxp3<SUP>+</SUP> regulatory T cells (Tregs), IL-17<SUP>+</SUP>CD4<SUP>+</SUP> Th17 cells, and CD11b<SUP>+</SUP>Ly-6C<SUP>hi</SUP> and Ly-6C<SUP>lo</SUP> monocytes. CD11c<SUP>hi</SUP> DC ablation resulted in the accumulation of IL-17<SUP>+</SUP>CD4<SUP>+</SUP> Th17 cells in the CNS, thereby leading to lower ratio of Tregs to Th17 cells. This result was corroborated by the higher expression levels of IL-17 and RORγT in CD4<SUP>+</SUP> T cells from the brains of CD11c<SUP>hi</SUP> DC-ablated mice. In addition, CD11c<SUP>hi</SUP> DC-ablated mice showed higher frequency and total number of inflammatory CD11b<SUP>+</SUP>Ly-6C<SUP>hi</SUP> monocytes, whereas CD11b<SUP>+</SUP>Ly-6C<SUP>lo</SUP> monocytes were detected with lower frequency and total number in CD11c<SUP>hi</SUP> DC-ablated mice. Furthermore, CD11c<SUP>hi </SUP>DC ablation altered the phenotype and function of CD11b<SUP>+</SUP>Ly-6C<SUP>lo</SUP> monocytes, resulting in lower levels of activation marker and anti-inflammatory cytokine (IL-10 and TGF-β) expression. Collectively, these results indicate that CD11c<SUP>hi</SUP> DC ablation caused an imbalance in CD4<SUP>+</SUP> Th17/Treg cells and CD11b<SUP>+</SUP>Ly-6C<SUP>hi</SUP>/Ly-6Clo monocytes in the lymphoid tissue and CNS during JE progression. This imbalanced orchestration of pro- and anti-inflammatory leukocytes following CD11c<SUP>hi</SUP> DC ablation may contribute to the exacerbation of JE.
목차
MATERIALS AND METHODS
INTRODUCTION
RESULTS AND DISCUSSION
REFERENCES
참고문헌 (26)
참고문헌 신청
Campbell, G. L., S. L. Hills, M. Fischer, J. A. Jacobson, C. H. Hoke, J. M. Hombach, A. A. Marfin, T. Solomon, T. F. Tsai, V. D. Tsu, and A. S. Ginsburg. 2011. Estimated global incidence of Japanese encephalitis: a systematic review. Bull. World Health Organ 89: 766-774E.
Ashhurst, T. M., C. Vreden, L. Munoz-Erazo, P. Niewold, K. Watabe, R. L. Terry, C. Deffrasnes, D. R. Getts, and N. J. Cole King. 2013. Antiviral macrophage responses in flavivirus encephalitis. Indian J. Med. Res. 138: 632-647.
Li, F., Y. Wang, L. Yu, S. Cao, K. Wang, J. Yuan, C. Wang, K. Wang, M. Cui, and Z. F. Fu. 2015. Viral infection of the central nervous system and neuroinflammation precede blood-brain barrier disruption during Japanese encephalitis virus infection. J. Virol. 89: 5602-5614.
Ye, J., R. Jiang, M. Cui, B. Zhu, L. Sun,Y . Wang, A. Zohaib, Q. Dong, X. Ruan, Y. Song, W. He, H. Chen, and S. Cao. 2014. Etanercept reduces neuroinflammation and lethality in mouse model of Japanese encephalitis. J. Infect. Dis. 210: 875-889.
Han, Y. W., J. Y. Choi, E. Uyangaa, S. B. Kim, J. H. Kim, B. S. Kim, K. Kim, and S. K. Eo. 2014. Distinct dictation of Japanese encephalitis virus-induced neuroinflammation and lethality via triggering TLR3 and TLR4 signal pathways. PLoS Pathog. 10: e1004319.
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UCI(KEPA) : I410-ECN-0101-2018-517-000885573