An atypical role for the myeloid receptor Mincle in central nervous system injury.
Document Type
Article
Publication Date
6-2017
JAX Location
Reprint Collection
JAX Source
J Cereb Blood Flow Metab 2017 Jun 37(6):2098-2111
Volume
37
Issue
6
First Page
2098
Last Page
2111
ISSN
1559-7016
PMID
27492949
DOI
https://doi.org/10.1177/0271678X16661201
Abstract
The C-type lectin Mincle is implicated in innate immune responses to sterile inflammation, but its contribution to associated pathologies is not well understood. Herein, we show that Mincle exacerbates neuronal loss following ischemic but not traumatic spinal cord injury. Loss of Mincle was beneficial in a model of transient middle cerebral artery occlusion but did not alter outcomes following heart or gut ischemia. High functional scores in Mincle KO animals using the focal cerebral ischemia model were accompanied by reduced lesion size, fewer infiltrating leukocytes and less neutrophil-derived cytokine production than isogenic controls. Bone marrow chimera experiments revealed that the presence of Mincle in the central nervous system, rather than recruited immune cells, was the critical regulator of a poor outcome following transient middle cerebral artery occlusion. There was no evidence for a direct role for Mincle in microglia or neural activation, but expression in a subset of macrophages resident in the perivascular niche provided new clues on Mincle's role in ischemic stroke. J Cereb Blood Flow Metab 2017 Jun 37(6):2098-2111.
Recommended Citation
Arumugam T,
Manzanero S,
Furtado M,
Biggins P,
Hsieh Y,
Gelderblom M,
MacDonald K,
Salimova E,
Li Y,
Korn O,
Dewar D,
Macrae I,
Ashman R,
Tang S,
Rosenthal N,
Ruitenberg M,
Magnus T,
Wells C.
An atypical role for the myeloid receptor Mincle in central nervous system injury. J Cereb Blood Flow Metab 2017 Jun 37(6):2098-2111