I think I mentioned this before. When you get inflammation, you get activation of the complement system. The complement system produces a compound called C3b which sticks to the pathogen. Phagocytes have receptors for C3b which allow the pathogen to be engulfed. Other times, antibodies will coat the pathogen and the phagocyte has receptors for these antibodies which help engulf it. Like this.
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This is called "opsonisation" (and it's not needed in VCE)
Finally, some bacteria also trigger some specific receptors on phagocytes which initiates phagocytosis.
No, other immune cells can also distinguish between self and non-self in other ways (ie through the PRRs on phagocytes, membrane-bound antibodies on B-cells). Only T-cells use MHC to distinguish between self and non-self.
Thanks guys, so is there a reason why the examiners report stated that immune cells recognise with MHC markers to distinguish from self and nonself? I was in a bit of a predicament because I assumed they were not wrong, and I assumed that all immune cells actually interacted with MHC markers to recognise them or not..
So different immune cells identify self from nonself in different ways, right?
T-Cells: bind with MHC II molecules ( and also MHC I via viral infected host cells? )
B-Cells: transmembrane antibodies specific to each antigen.
Phagocytes: Some receptor mechanism that is not explored within VCE Bio?
Cheers guys, and I really appreciate your help all morning, must have asked the same question over and over again, but hopefully if the above is correct, then at least it worked, right? xD
Edit: If all nucleated cells possess MHC I markers with self-antigens presented on them, and if only T-cells interract with MHC molecules, then how do phagocytes bypass them?