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首页> 外文期刊>Proceedings of the National Academy of Sciences of the United States of America. >IL-1 beta enables CNS access to CCR2(hi) monocytes and the generation of pathogenic cells through GM-CSF released by CNS endothelial cells
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IL-1 beta enables CNS access to CCR2(hi) monocytes and the generation of pathogenic cells through GM-CSF released by CNS endothelial cells

机译：IL-1 beta enables CNS access to CCR2(hi) monocytes and the generation of pathogenic cells through GM-CSF released by CNS endothelial cells

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Molecular interventions that limit pathogenic CNS inflammation are used to treat autoimmune conditions such as multiple sclerosis (MS). Remarkably, IL-1 beta-knockout mice are highly resistant to experimental autoimmune encephalomyelitis (EAE), an animal model of MS. Here, we show that interfering with the IL-1 beta/IL-1R1 axis severely impairs the transmigration of myeloid cells across central nervous system (CNS) endothelial cells (ECs). Notably, we report that IL-1 beta expression by inflammatory CCR2(hi) monocytes favors their entry into the spinal cord before EAE onset. Following activation with IL-1 beta, CNS ECs release GM-CSF, which in turn converts monocytes into antigen-presenting cells (APCs). Accordingly, spinal cord-infiltrated monocyte-derived APCs are associated with dividing CD4(+) T cells. Factors released from the interaction between IL-1 beta-competent myeloid cells and CD4(+) T cells are highly toxic to neurons. Together, our results suggest that IL-1 beta signaling is an entry point for targeting both the initiation and exacerbation of neuroinflammation.

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