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Chapter 2

BIO120H1 Chapter Notes - Chapter 2: C-Reactive Protein, Factor H, Conformational Change

Course Code
Bebhinn Treanor

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Chapter 2
Extracellular infections-pathogens live and replicate in spaces btw human
o Accessible to soluble molecules of immune system
Intracellular infections-pathogens replicate inside human cells
o Not accessible to soluble molecules of immune system
o Pathogens that live in nucleus or cytosol can be attacked by killing the
infected cell
o Pathogens that live in intracellular vesicles can be attacked by
activating the infected cell to intensify its antimicrobial activity
Vast majority of human infections come from transmission of pathogen
either direct or indirect from another person already infected
Anthrax is spread by spores that are resistant to heat and dessication so they
can go long distances.
HIV is sensitive to enviro changes, passed btw ppl by intimidate contact
As soon as pathogen penetrates epithelial barrier and starts to live in human
tissue, innate immunity starts.
o Liver makes complement which coats the surface of bacteria and
extracellular virus particles and makes it easier to phagocytosize
Many complement components are proteolytic enzymes, proteases that
circulate in inactive forms=zymogens
Infection triggers complement activation
o Each protease cleaves and activiates the next enzyme in path
o Each protease is highly specific for complement component it cleaves
and cleaves at signle site
o Usually serine protease, involves digestive enzymes trypsin and
C3 (complement component 3) is most important
o Patients lacking C3 are prone to successive severe infections
o When complement activated by infection, it cleaves C3 into small C3a
and large C3b…some C3b covalently bonds to pathogen
surface=complement fixation
o Bound C3b tags pathogen for destruction by phagocytes and also
organizes formation of protein complexes that damage the pathogens
o C3a acts as chemoattractant to recruit effector cells, including
phagocytes form blood to infection
C3 has high energy thioester bond
o C3 is made and enters circulation in inactive form, where the thioester
is sequestered and stabilized within the hydrophobic interior of
o When C3 is cleaved into C3a and C3b, the bond is exposed and is
nucleophilic attacked by water or AA and hydroxyl groups of proteins
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