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
CD4 t cells differentiate into
TH1 cells
what cause the differentiation of CD4 t cells into TH1
il-12
how can phagocytosed bacteria stimulate cd8 t cells
if bacterial antigens are transported into the cytosol
the macrophage activation that occurs in response to intracellular micrboes can also cause what
tissue damage
induce delayed type hypersensitivty
when bacteria presist for long periods within phagocytes and cause chronic antigen stimulation resulting in the formation of granulomas
tuberculosis results from infection by what
intracellular pathogens
patients that have high antibody titers but weak cell mediated immune responses mycobacteria proliferate and macrophage activation results in destructive lesions
lepromatous leprosy
patients develop stron cell mediated immunity with less tissue destruction and reduced bacterial growth
tuberculoid leprosy
what is the most important factor with fungal infections
compromised immunity
neutrophil deficiencys can
cause a predisposition to fungal infections
where can fungi live
extracellular tissues and within phagocytes
what is the primary mediators of fungal infection
neutrophils and macrophages
fungi causes a strong response from what
TH17
what are important for killing of virus infected cells
type 1 interferons and nk cell
what triggers ifn production in viral responce
recognition of viral nucleic acids by TLRs and RIG-1
how can nk cells recognize virally infected cells
decreased class 1 mhc expression
secretion of igA can do what to viral infections
neutralize viruses that enter through the mucosal system
CTLs do what
kill cells infected by viruses
CTLs recognize what
viral peptides presented by MHC 1
Latent infections
viral DNA persists in host cells but virus does not replicate or kill host cells
how can viruses evade immune cells
alter their antigens by surface glycoprotiens undergoing antigenic variation through point mutation or reassortment of RNA segments
some viruses can inhibit what
MHC 1 associated presentation of cytosolic protein antigens
pxviruses
produce molecules that bind and block the activity of cytokines and chemokines
epstein barr
produces a protein similar to IL-10 that supresses immune response
how does hiv survive
by infecting and eliminating CD4 t cells
why are most parasitic infections chronic
weak innate immunity and the ability to evade adaptive immune responses
parasitic infections activate what kind of immunity
innate
helminths are able to avoid immune responses due to
teguments that make them resistant to the cytocidal mechanisms of phagocytes adn develop resistance to complement mediated lysis
what is the defense mechanism against protozoa
cell mediated immunity specifically the activation of macrophages by th1 cytokines
what causes malaria
plasmodium
what serves as a vector for malaria
female anopheles mosquito
what cycle of plasmodium enters through mosquito bite
sporozites
plasmodium sporozites in the liver transform into what
merozoites
merozites infect what
red blood cells
what is the difficulty with immune response to malaria
antibodies are only effective against a specific life stage
CLTs can kill what kinda malaria
sporozoite infected hepatocytes
how do cd8 t cells kill sporozite infected hepatocytes
they secrete ifn-y to activate hepatocytes to produce NO to kill parasites
what cells mediate helminth infections
th2
how do th2 cells responde to helminth infections
production of IgE and activation of eosinophiles
what recruits eosinophils to helminth infectiins
IgE and IgA
th2 cells produce what that helps with the development of eosinophils
IL-4
how do parasites evade protective immunity
reducing their immunogenicity and inhibiting host immune response
sporozite stage of malaria differ how from the merozite stage
antigenically
why is it difficult to design an effective vaccine against trypanosomes
antigenic variation
what stage of development must be targeted in plasmodium to prevent the infection of liver cells
sporozoites
what is an innate immunity mechanism for eradicating established viral infections
NK cells
what is not a part of the innate immune response to extracellular bacteria
nk cell activation
what are a part of the innate immune response to extracellular bacteria
complement activation by LPS and mannose, activation of phagocytes by TCR, inflmation
what is an adaptive immunity mechanism for eradicating an established viral infection
CD8 t cells
antigenic variation allows for the evasion of what type of immune recognition
antibody recognition of microbial surface molecules
what is an adaptive immunity mechanism for preventing viral infection
antibodies which can neutralize viruses before they infect cells
what is the main mechanism of adaptive immunity to fungi
cell mediated immunity
extra cellular fungi produce a repsonse from what cells
th17`
fungal products activate what cells
dendritic cells
dendritic cells that are stimulated by fungi products produce what
IL-6 and IL-23
what mediates the innate immune response to intracellular bacteria
nk cells
macrophages produce what to activate nk cells
IL-12 and IL-15
TSST-1 is presented by what
MHC 2 to t cells that have a tcr v-beta gene segment
TSST-1 presentation by mhc 2 causes what
polyclonal activation of many t cells and a large release of inflammatory cytokines
what immune evasion strategy does influenza use
antigenic variation
