Abstract
The very simplistic view that inflammation in multiple sclerosis (MS) is tout court detrimental has to be profoundly reconsidered. Experimental evidence strongly supports the concept that inflammation in MS is aimed not only at destroying and phagocytosing damaged (infected?) cells (detrimental phase) but also at promoting tissue regeneration or tissue repair via scar formation (resolution or protective phase). Microglia seem to play a crucial role in the different inflammatory phases in MS because they move through multiple functional levels (quantum jumps) either to remove the "danger" signal or to restore the integrity of the central nervous system. The understanding of the molecular signature of any of the quantum microglial states could be useful to better define the cellular and molecular mechanisms underling the different phases of inflammation in MS. This could contribute not only to the design of better therapeutic drugs, but also to the comprehension of the shortcomings of currently used anti-inflammatory drugs.
| Original language | English |
|---|---|
| Pages (from-to) | 39-44 |
| Number of pages | 6 |
| Journal | Journal of Neuroimmunology |
| Volume | 191 |
| Issue number | 1-2 |
| DOIs | |
| Publication status | Published - Nov 2007 |
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Keywords
- Inflammation
- Microglia
- Multiple sclerosis
- Quantum states
- Regeneration
ASJC Scopus subject areas
- Immunology
- Immunology and Allergy
- Clinical Neurology
- Neurology
Cite this
Multifaceted aspects of inflammation in multiple sclerosis : The role of microglia. / Muzio, Luca; Martino, Gianvito; Furlan, Roberto.
In: Journal of Neuroimmunology, Vol. 191, No. 1-2, 11.2007, p. 39-44.Research output: Contribution to journal › Article
}
TY - JOUR
T1 - Multifaceted aspects of inflammation in multiple sclerosis
T2 - The role of microglia
AU - Muzio, Luca
AU - Martino, Gianvito
AU - Furlan, Roberto
PY - 2007/11
Y1 - 2007/11
N2 - The very simplistic view that inflammation in multiple sclerosis (MS) is tout court detrimental has to be profoundly reconsidered. Experimental evidence strongly supports the concept that inflammation in MS is aimed not only at destroying and phagocytosing damaged (infected?) cells (detrimental phase) but also at promoting tissue regeneration or tissue repair via scar formation (resolution or protective phase). Microglia seem to play a crucial role in the different inflammatory phases in MS because they move through multiple functional levels (quantum jumps) either to remove the "danger" signal or to restore the integrity of the central nervous system. The understanding of the molecular signature of any of the quantum microglial states could be useful to better define the cellular and molecular mechanisms underling the different phases of inflammation in MS. This could contribute not only to the design of better therapeutic drugs, but also to the comprehension of the shortcomings of currently used anti-inflammatory drugs.
AB - The very simplistic view that inflammation in multiple sclerosis (MS) is tout court detrimental has to be profoundly reconsidered. Experimental evidence strongly supports the concept that inflammation in MS is aimed not only at destroying and phagocytosing damaged (infected?) cells (detrimental phase) but also at promoting tissue regeneration or tissue repair via scar formation (resolution or protective phase). Microglia seem to play a crucial role in the different inflammatory phases in MS because they move through multiple functional levels (quantum jumps) either to remove the "danger" signal or to restore the integrity of the central nervous system. The understanding of the molecular signature of any of the quantum microglial states could be useful to better define the cellular and molecular mechanisms underling the different phases of inflammation in MS. This could contribute not only to the design of better therapeutic drugs, but also to the comprehension of the shortcomings of currently used anti-inflammatory drugs.
KW - Inflammation
KW - Microglia
KW - Multiple sclerosis
KW - Quantum states
KW - Regeneration
UR - http://www.scopus.com/inward/record.url?scp=35848957483&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=35848957483&partnerID=8YFLogxK
U2 - 10.1016/j.jneuroim.2007.09.016
DO - 10.1016/j.jneuroim.2007.09.016
M3 - Article
VL - 191
SP - 39
EP - 44
JO - Journal of Neuroimmunology
JF - Journal of Neuroimmunology
SN - 0165-5728
IS - 1-2
ER -