mediated by antibodies (from B cells) to target extracellular pathogens
Cell-mediated response
cytotoxic T cells to target virus-infected cells.
Ig
immunoglobulin
affinity
the binding strength of one antigen binding site
avidity
the combined strength of two or more antigen binding site
crosslinking
facilitate removal by phagocytic cells such as macrophages
IgG
neutrophils, macrophages, facilitates phagocytosis of pathogens
IgE
Mast cells, eosinophils, immune response to parasites and allergy
IgA
epithelial cells, mucosal immunity secretions
IgM
the first antibody to be secreted in an immune response, but is not very efficient
IgD
expressed in mature B cells at the same time as IgM, it is mainly exposed as a receptor on the cell surface and very little is secreted as antibody
TH2 cells
stimulate immunoglobulin class switching in B cells to produce IgE and recruit mast cells and eosinophils
allergies
inappropriate TH2 responses: involve antibodies of the IgE class, mast cells, and eosinophils
neutralization
binding on antibodies to bacterial toxins or viruses prevents them from attacking cells by blocking the binding site they normally use to attach to cells
opsonization
coating bacteria or other pathogens with proteins such as antibodies facilitates their removal by phagocytic cells such as neutrophils and macrophages
IgG
the main antibody isotype used in opsonization
TH1 cells
promotes Ig class switching from IgM to IgG
IgG receptors
bind to the IgG and tethers the pathogen to the surface of the cells
clustering of IgG receptors
activating signals that stimulate phagocytosis and cell activation
flexible hinge region
allows antibody to bind with both arms to many different arrangements of antigens on the surface of pathogens
bigger hinge region
more flexible and efficient at binding to pathogens, but also becomes more susceptible to proteolytic attack that limits its lifetime
smaller hinge region
have a long lifetime because they are less susceptible to proteolytic attack
complement proteins
blood proteins that are activated by a proteolytic cascade following antibody binding to antigens on pathogens
proteolytic conversion of complement C3
produces C3b which adds another layer of opsonization
C3b receptors
combine with Fc receptors for antibodies to enable more efficient phagocytosis of bacteria
classical pathway
initiated by binding of complement C1 to antibodies, so it depends on an adaptive immune response
C1q
binds to antibody on pathogens
C1r
protease that cleaves and activated C1s
C1s
protease that cleaves C4 and C2
formation of C3b
opsonizes pathogens, the main goal of the complement pathway
activation of C1
leads to subsequent activation of C2 and C4 which form the C3 convertase that generates C3b
C3b
opsonizes pathogens and also activates the membrane attack complex
complement C5b-C9
form a membrane-attack complex that kills bacteria by creating a lytic pore in the membrane
C3a, C4a, C5a
stimulate leukocyte recruitment
C5a
has the strongest activity
C4a
has the weakest activity
C1
binds to IgG to IgM antibodies and initiates the complement cascade
C4b and C2a
combine to form the C3 convertase
C3b
the major opsonin that facilitates phagocytosis
C3a, C4a, C5a
functions as important inflammatory mediators in leukocyte recruitment and are referred to as anaphylatoxins