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15 Cards in this Set

  • Front
  • Back

Acute inflammation

Local reaction


Movement of protein and cells from blood to tissue


Predominantly neutrophils

What enzymes kills neutrophils

Myeloperoxidase

C3a

Adhesion molecules on blood vessel walls


Sticky so causes neutrophils to slow down


Eventually lots of adhesion molecule near infection eventually stops

Neutrophils in responses to adhesion molecules

Neutrophils can move out of blood due to increased vascular permeability follow cytokines

C3a and c5a

Activate mast cell

Mast cell function

Resident in tissue


Release of vasoactive amines


Release of cytokines

Inflammatory

Cytokines


Chemokines


Complement


Amines

Chronic granulomasdisease

Mutations in genes for NADPH oxidase


No respiratory burst


No ph change in phagosome


No damage to pathogens


Infections are not cleared

Inflammatory cytokines stimulate production of acute phase protein

Stimulate production of CRP and MBP

CRP binds to

Bacterial and fungal cell walls

C4 binds to mbl

C4 gets cleaved


C4b attaches to cell and binds 2a


Together this can cleave C3

CRP

Makes c3 convertase

Infected cells produce IFN-a and IFN -B this produces the response of

Induce resistance to viral replication


Increase expression of ligands for receptors on NK cells


Activate cells to kill virus infected cells

NK cells

Large granular lymphocytes


Activity increases 20-100 times on exposure to the interferons


NK provide an early response to virus infection until cytokines cells

How is NK killing controlled

Normal cells have receptors that inhibit NK that damages cells don’t have


Infected cells have nkg2d ligands that bind to receptor on NK