期刊
IMMUNITY
卷 46, 期 2, 页码 245-260出版社
CELL PRESS
DOI: 10.1016/j.immuni.2017.01.007
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资金
- Swiss National Science Foundation [316030_150768, 310030_146130, CRSII3_136203]
- European Union [279017, 316722, 602239]
- Swiss Multiple Sclerosis Society
- University of Zurich [54311803]
- Koetser Foundation
- Austrian Academy of Science
- Swiss National Science Foundation (SNF) [CRSII3_136203] Funding Source: Swiss National Science Foundation (SNF)
Chronic inflammatory diseases are influenced by dysregulation of cytokines. Among them, granulocyte macrophage colony stimulating factor (GMCSF) is crucial for the pathogenic function of T cells in preclinical models of autoimmunity. To study the impact of dysregulated GM-CSF expression in vivo, we generated a transgenic mouse line allowing the induction of GM-CSF expression in mature, peripheral helper T (Th) cells. Antigen-independent GM-CSF release led to the invasion of inflammatory myeloid cells into the central nervous system (CNS), which was accompanied by the spontaneous development of severe neurological deficits. CNS-invading phagocytes produced reactive oxygen species and exhibited a distinct genetic signature compared to myeloid cells invading other organs. We propose that the CNS is particularly vulnerable to the attack of monocyte-derived phagocytes and that the effector functions of GM-CSF-expanded myeloid cells are in turn guided by the tissue microenvironment.
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