PT  - JOURNAL ARTICLE
AU  - Claude, Janine
AU  - Linnartz-Gerlach, Bettina
AU  - Kudin, Alexei P.
AU  - Kunz, Wolfram S.
AU  - Neumann, Harald
TI  - Microglial CD33-Related Siglec-E Inhibits Neurotoxicity by Preventing the Phagocytosis-Associated Oxidative Burst
AID  - 10.1523/JNEUROSCI.2211-13.2013
DP  - 2013 Nov 13
TA  - The Journal of Neuroscience
PG  - 18270--18276
VI  - 33
IP  - 46
4099  - http://www.jneurosci.org/content/33/46/18270.short
4100  - http://www.jneurosci.org/content/33/46/18270.full
SO  - J. Neurosci.2013 Nov 13; 33
AB  - Sialic acid-binding Ig-like lectins (Siglecs) are members of the Ig superfamily that recognize sialic acid residues of glycoproteins. Siglec-E is a mouse CD33-related Siglec that preferentially binds to sialic acid residues of the cellular glycocalyx. Here, we demonstrate gene transcription and protein expression of Siglec-E by cultured mouse microglia. Siglec-E on microglia inhibited phagocytosis of neural debris and prevented the production of superoxide radicals induced by challenge with neural debris. Soluble extracellular Siglec-E receptor protein bound to the neural glycocalyx. Coculture of mouse microglia and neurons demonstrated a neuroprotective effect of microglial Siglec-E that was dependent on neuronal sialic acid residues. Increased neurotoxicity of microglia after knockdown of Siglece mRNA was neutralized by the reactive oxygen species scavenger Trolox. Data suggest that Siglec-E recognizes the intact neuronal glycocalyx and has neuroprotective function by preventing phagocytosis and the associated oxidative burst.