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 |
|---|---|
| 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 |
Funding
Work in the authors' laboratories is supported by grants of the Deutsche Forschungsgemeinschaft (MS: SCHW 416/7-1 , SJ and MG: JA 690/8-1 ) and the European Union's Seventh Framework Programme FP7 under grant agreement 607962 to MS (nEUROinflammation).
Research Areas and Centers
- Academic Focus: Center for Brain, Behavior and Metabolism (CBBM)
