2016年9月
Lung inflammation stalls T-h 17-cell migration en route to the central nervous system during the development of experimental autoimmune encephalomyelitis
INTERNATIONAL IMMUNOLOGY
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- ,
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- 巻
- 28
- 号
- 9
- 開始ページ
- 463
- 終了ページ
- 469
- 記述言語
- 英語
- 掲載種別
- 研究論文(学術雑誌)
- DOI
- 10.1093/intimm/dxw013
- 出版者・発行元
- OXFORD UNIV PRESS
Recruiting pathogenic T cells to the central nervous system (CNS) is a critical step during the development of experimental autoimmune encephalomyelitis (EAE). Here, we report that the absence of autophagy and microtubule-associated protein 1A/1B-light chain 3-associated phagocytosis significantly delayed the onset of EAE in Atg7 conditional knockout (Atg7 CKO) mice in myeloid cells. T-helper cell- cell priming appeared to be normal in the Atg7 CKO mice, but the mice showed significant accumulation of T-h 17 cells in the lung. The data suggested that the stalling of T h 17 cells in the lung en route to the CNS caused the delay. The lung of Atg7 CKO mice, in which we previously demonstrated spontaneous mild inflammation, showed high expression of CCL20, a chemokine that attracts T-h 17 cells. We have also shown that LPS intranasal instillation delayed EAE onset, suggesting that pulmonary inflammation has an impact on EAE development. Based on our data, therapeutic immunomodulation targeted to the lung, rather than systemically, might be a possible future option to treat multiple sclerosis.
- リンク情報
- ID情報
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- DOI : 10.1093/intimm/dxw013
- ISSN : 0953-8178
- eISSN : 1460-2377
- PubMed ID : 26989091
- Web of Science ID : WOS:000385016500005