Abstract
The interaction between a microorganism and a potential host may modify each other in multiple ways. Because of their central role in controlling leukocyte trafficking and activation, chemokines may be essential in defining these interactions. Here, we describe potential uses of intravital microscopy to define the role of chemokines and their receptors in the context of HSV-1 infection and EAE. We show that CCL5 plays a major role in driving neuropathology by mediating leukocyte adhesion and consequent migration in HSV-1 encephalitis. In contrast, CCR5 is important to attract cell types that modulate negatively CNS damage at the cost of allowing greater viral replication in the brain. Finally, intravital microscopy studies were crucial to determine that induction of leukocyte adhesion and subsequent emigration into the CNS is a major mechanism of action of CCL2 in EAE.
Original language | English (US) |
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Pages (from-to) | 62-65 |
Number of pages | 4 |
Journal | Journal of Neuroimmunology |
Volume | 224 |
Issue number | 1-2 |
DOIs | |
State | Published - Jul 2010 |
Externally published | Yes |
Keywords
- Chemokines
- Experimental autoimmune encephalomyelitis
- HSV-1
- Intravital microscopy
- Neuroinflamamation
ASJC Scopus subject areas
- Immunology and Allergy
- Immunology
- Neurology
- Clinical Neurology