Presenting lipid antigens
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《细胞学杂志》
Lipids circulate as part of large particles containing apolipoproteins such as ApoE. Cells that need more lipids secrete ApoE, which grabs onto fats and is then recaptured via receptor-mediated endocytosis. Brenner noticed that dendritic cells were dumping out much more ApoE than is required for their metabolic needs for fats.
But much of this ApoE is probably used to search for foreign lipids, according to the findings. The authors show that ApoE binds directly to lipid antigens and brings them into dendritic cells much more efficiently than does macropinocytosis (which dendritic cells use to engulf foreign peptides). Endocytosis "deposits the lipids in endosomal compartments," says Brenner, "right where CD1 is waiting. Then they come to the surface, where they can activate T cells."
In the absence of ApoE, dendritic cells required hours rather than minutes in contact with lipid antigens to activate T cells. This lag is precious lost time during which a pathogen might be rapidly multiplying. Blocking ApoE-dependent endocytosis might be beneficial, however, in preventing lipid-filled macrophages from initiating autoimmune disorders such as atherosclerosis.
Reference:
van den Elzen, P., et al. 2005. Nature. 437:906–910.(Immune cells inspect not just protein bu)
But much of this ApoE is probably used to search for foreign lipids, according to the findings. The authors show that ApoE binds directly to lipid antigens and brings them into dendritic cells much more efficiently than does macropinocytosis (which dendritic cells use to engulf foreign peptides). Endocytosis "deposits the lipids in endosomal compartments," says Brenner, "right where CD1 is waiting. Then they come to the surface, where they can activate T cells."
In the absence of ApoE, dendritic cells required hours rather than minutes in contact with lipid antigens to activate T cells. This lag is precious lost time during which a pathogen might be rapidly multiplying. Blocking ApoE-dependent endocytosis might be beneficial, however, in preventing lipid-filled macrophages from initiating autoimmune disorders such as atherosclerosis.
Reference:
van den Elzen, P., et al. 2005. Nature. 437:906–910.(Immune cells inspect not just protein bu)