Module 11 Flashcards
extracellular bacteria cause disease by
inducing inflammation which results in tissue destruction at the site of infection and producing toxins such as endotoxins or exotoxins
the principal mechanisms of innate immunity are
complement activation, phagocytosis, and the inflammatory response
what activates the alternative complement pathway
LPS in the cell walls of gram negative bacteria
what activates the lectin complement pathway
mannose expressing bacteria
TLR and FC receptor signaling can induce what
the production of cytokines and acute phase proteins
what part of the alternative pathway binds to the microbe cell
c3b
what is the c3 convertase of the alternative pathway
c3bBb
what is the c5 convertase of the alternative pathway
c3bBbc3bc5
lectin pathway initiation
binding of mannose to mannose binding lectin
what is the c3 convertase of the lectin pathway
c4b2a
what is the c5 convertase of the lectin pathway
c4b2ac3bc5
killing of phagocytosed microbes is done by what
ROS and NO
the principal protective immune response functions to block infection, eliminate microbes, and neutralize toxins
humoral immunity
polysaccharide ig
igm
protein ig
iga igg
what are effector mechanisms
phagocytosis, classical complement pathway, IgM and IgG and neutrailization
protein antigens from extracellular bacteria can activate what
cd4 helper t cells
TH1 generates what
IFN-y
TH17 mediates what
responses that eliminate extracellular microbes
IL-17 does what
causes inflamation
IFN-y does what
activates macrophages to phagocytoes and kill bacteria
what are the consequences of host response to extracellular bacteria
inflammation and spetic shock
what causes septic shock
disseminated infections by gram neg bacteria
what is the principal mediator of septic shock
TNF, IFN-y and IL-12
viral or bacterial proteins that bind simultaneously to Vb domain of TCR and the alpha chain of class 2 MHC molecule
superantigens
exogenous
exotoxins
endogenous
viral proteins
Activation by superantigens is
polyclonal
what is polyclonal
superantigens bind outside the tcr antigen binding cleft and affect a large number of t cells
protective immunity
activation of peptide x specific t cell clones only
super antigen binding to mhc 2
polyclonal activation of vb3 t cells causing cytokine storm and deletion of t cells
what causes rhematic fever
pharyngeal infections with some type of beta hemolytic streptococci
pharyngeal infections cause
production of antibodies against bacterial cell wall protein m
m protein antibodies do what
cross react with myocardial proteins and deposit in the heart causing inflammation and damage
intracellular bacteria can do what
survive and replicate within phagocytes where they are inacessable to antibodeis
how do intracellular bacteria activate nk cells
they induce expression of nk activating ligands on infected cells or stimulate the production of IL-12 by DCs and macrophages
NK cells produce IFN-gamma which does what
activates macrophages
macrophages infected with microbes produces what which actives nk cells to produce what which stimulates macrophages to kill phagocytosed microbes
IL-12 IFN-y
how do t cells activate macrophages
through CD40 signaling and IFN-y