Abstract:
:Interleukin-1 (IL-1) signaling is important for multiple potentially pathogenic processes in the central nervous system (CNS), but the cell-type-specific roles of IL-1 signaling are unclear. We used a genetic knockin reporter system in mice to track and reciprocally delete or express IL-1 receptor 1 (IL-1R1) in specific cell types, including endothelial cells, ventricular cells, peripheral myeloid cells, microglia, astrocytes, and neurons. We found that endothelial IL-1R1 was necessary and sufficient for mediating sickness behavior and drove leukocyte recruitment to the CNS and impaired neurogenesis, whereas ventricular IL-1R1 was critical for monocyte recruitment to the CNS. Although microglia did not express IL-1R1, IL-1 stimulation of endothelial cells led to the induction of IL-1 in microglia. Together, these findings describe the structure and functions of the brain's IL-1R1-expressing system and lay a foundation for the dissection and identification of IL-1R1 signaling pathways in the pathogenesis of CNS diseases.
journal_name
Immunityjournal_title
Immunityauthors
Liu X,Nemeth DP,McKim DB,Zhu L,DiSabato DJ,Berdysz O,Gorantla G,Oliver B,Witcher KG,Wang Y,Negray CE,Vegesna RS,Sheridan JF,Godbout JP,Robson MJ,Blakely RD,Popovich PG,Bilbo SD,Quan Ndoi
10.1016/j.immuni.2018.12.012subject
Has Abstractpub_date
2019-02-19 00:00:00pages
317-333.e6issue
2eissn
1074-7613issn
1097-4180pii
S1074-7613(18)30560-0journal_volume
50pub_type
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