Abstract
Hematogenous recruitment of monocytes and macrophages has traditionally been viewed as a harmful process causing exacerbation of brain injury after stroke. However, emerging findings suggest equally important protective features. Inflammatory monocytes are rapidly recruited to ischemic brain via a CCR2-dependent pathway and undergo secondary differentiation in the target tissue towards non-inflammatory macrophages, mediating neuroprotection and repair of the ischemic neurovascular unit. In contrast, independent recruitment of non-inflammatory monocytes via CX3CR1 does not occur. Thus, protective features of hematogenous macrophages mainly depend on initial CCR2-dependent cell recruitment. Under therapeutic considerations, specific modulation of monocyte-derived macrophages will therefore be more appropriate than non-selectively blocking their hematogenous recruitment. This article is part of a Special Issue entitled: Neuro Inflammation edited by Helga E. de Vries and Markus Schwaninger.
Original language | English |
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Journal | Biochimica et Biophysica Acta - Molecular Basis of Disease |
Volume | 1862 |
Issue number | 3 |
Pages (from-to) | 329-338 |
Number of pages | 10 |
ISSN | 0925-4439 |
DOIs | |
Publication status | Published - 01.03.2016 |
Research Areas and Centers
- Academic Focus: Center for Brain, Behavior and Metabolism (CBBM)