A
full innate immune system (e.g. complement system, scavenger receptors,
Toll-like receptors (TLR)) has been described in the CNS and is thought
to be an extremely efficient army designed to fight against invading
pathogens and toxic cell debris such as apoptotic cells and amyloid
fibrils. The binding of soluble or secreted innate immune molecules on
pathogen-associated molecular patterns (PAMPs) as well as apoptotic
cell-associated molecular patterns (ACAMPs) provide several “eat me”
signals to promote the safe disposal of the intruders by professional
and amateur phagocytes. These patterns are deciphered by receptors
(pattern recognition receptors, PRRs; e.g. CR3) that control
phagocytosis and associated inflammatory response depending on the
meaning of these signals. Importantly, in order to avoid excessive
collateral damage of surrounding cells, it is increasingly evident that
“don’t eat me” signals (coined herein as self-associated molecular
patterns, SAMPs; e.g. complement regulatory proteins, CD200) are of
paramount importance to signal a robust anti-inflammatory response and
promote tissue repair. Further knowledge of the innate immune response
in the CNS will greatly help to delineate the novel therapeutic routes
to protect from CNS inflammation and neurodegeneration.
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