Immunity to Infxn (Davis) Flashcards
Innate immunity to infxn?
- physical barriers
- phagocytosis
- complement
- inflammatory response
Antimicrobial peptides & proteins under innate immunity?
- alpha defensins
- beta defensins
- lysozyme
- cathelicidins
- collectins
- pentraxins
What is pus made out of?
dead neutrophils and pathogens
In inflammation, what are recruited to the site of infxn?
neutrophils and monocytes
Inflammation is a common & effective way to fight pyogenic bacteria, generally ____ bacteria
encapsulated
In the case that local inflammation cannot contain infxn, ___ from tissue macrophages can enter bloodstream & induce acute phase response
cytokines
in acute phase response, cytokines can result in what?
fever, hematopoiesis of neutrophils & monocytes, CRP production and defensins
What cells secrete cytokines that activate more macrophages?
Th1 cells
Complement activation is an alternative pathway activated quickly due to..?
due to natural turnover of C3
___ promote inflammation and wound healing
platelets
some pathogens such as _____ initiate coagulation/clotting themselves to protect against complement or abs!
S. aureus (coagulase enzyme)
adaptive immunity is initiated in..?
secondary lymphoid organs
the type of adaptive response generated depends on what..?
the type of pathogen and which cytokines are produced
what occurs in the secondary lymphoid organs?
antigen presentation and linked recognition
The main protective innate mechanisms to fight extracellular bacteria are:
- complement activation
- opsonization
- cytokines
- inflammation
Complement activation helps generates ___
opsonins
what can cytokines do?
cause the up regulation of selectins and adhesins for extravasation and fully activate macrophages
which complement products along w/ cytokines help recruit neutrophils and monocytes to promote inflammation and removal of pathogens?
C5a, C3a, C4a
The main protective adaptive mechanisms to fight extracellular bacteria involve antibody responses:
- T dependent/independent responses
- Th17 cells
T dependent responses are going to result in all isotypes being made! What occurs during early and late stage?
early- complement activation (IgM)
late- “noc”
___ cells are the main T cells involved in an extracellular bacteria infxn
Th17 cells
main mechanism induced by Th17 cells is..?
secretion of cytokines that induce an inflammatory response via extravasation of neutrophils and monocytes
Response can be T-independent esp if pathogen has what..?
polysacc. capsule
What pathogen has a capsule and what does a capsule do..?
H.influenzae; can activate B cells independently–> increased IgM
T-independent bacteria initiate an adaptive response that is mediated by…?
by activation of the classical complement pathway to induce opsonization or lysis
Our adaptive response to what bacteria involves T-independent–> increased IgM–> complement activation–> opsonization?
S. pneumoniae
The main protective innate mechanisms to fight intracellular bacteria:
- phagocytosis
- opsonization
Opsonization or phagocytosis result in production of?
IL-12 and IL-15 which stimulate NK cells
NK cells produce IFN-g which activate..?
macrophages
Main effector mechanism for intracellular bacteria is a…?
cell mediated response
(T/F) Abs and complement can’t reach bacteria inside cells but can be useful when bacteria become extracellular
TRUE
Which pathogens remain within the phagolysosome bc they have developed mechanisms to avoid being killed by oxidative burst?
intravesicular pathogens
which bacteria are known as intravesicular pathogens?
Mycobacterium and Legionella
Intravesicular bacteria stimulated phagocyte to produce ___ to direct differentiation of Th1 cells
IL-12
2 ways that Th1 cells activate macrophages to increase their ability to kill pathogens via oxidative burst?
- they interact w/ macrophages via CD40-CD40L pathway
2. Th1 cells secrete IFN-g
Some bacteria escape from the phagosome into the cytosol which puts bacteria in which pathway?
MHC class I pathway which results in activation of CD8+ T cells into CTLs
Which bacteria is known to escape into cytoplasm (cytosolic)?
listeria monocytogenes
main mechanism for innate immunity to fungal pathogens is ___
opsonization & intracellular killing via oxidative burst
___ is most important response to intracellular fungi infxns
CMI
Extracellular fungi result in differentiation of what cells?
Th17 cells
When a cell becomes infected w/ virus, it begins to secrete type I cytokines which include:
IFN-a and IFN-B
Some viruses suppress expression of MHC class I molecules and are killed by ..?
NK cells
IFN-a and IFN-B are induced by the presence of viral “signatures” such as ____ by intracellular PRRs
dsRNA
Type I interferons act in a paracrine manner to do what..?
to “warn” still healthy neighboring cells to prepare for viral infxn
Type I interferons up regulate of what for presentation?
MHC class I & TAP
Type I interferon produce enzymes to do what?
degrade viral RNA
(T/F) Type I interferons are produced by a cell after it gets infected by a virus
True
Type I interferons cause inactivation of ___ to prevent protein synthesis
eIF-2
Opsonization via C3b helps fight __ viruses while MAC lysis fights __ viruses
naked/enveloped
__ dominate primary response in adaptive viral immunity
CTLs
____ immunity dominates secondary response- before virions gain entry into cells and as they exit to find new cells
Humoral
(T/F) “noca” plays a role in adaptive response to viruses
FALSE; only “noc”
Once virions become intracellular, ___ is needed to eliminate them?
CMI
what occurs in early primary response for adaptive immunity against viruses?
- alternative complement
- viral antigens presented on MHC classes
- CD8+ T cells become CTLs
- Th17 secrete IFN-g–> NK cells
What occurs in late primary response for adaptive immunity against viruses?
- B cells become activated and produce IgM abs
- IgM activates classical complement
- complement products can opsonize or lyse virions
What occurs in secondary adaptive response to viruses?
- memory B cells plasma cells
- CTLs kill infected cells
- abs are useful as new virions escape infected cell
(T/F) many parasitic infxns become chronic and frequently do NOT result in development of complete immunological protection
True!
Protozoan parasitic infxns are mediated by __ and ___ w/ killing via oxidative burst
PRRs and phagocytosis
Helminthic parasitic infxns release ___ enzymes and activate alternative complement MAC lysis
lytic
Protozoa such as ___ require both humoral and CMI
plasmodium falciparum
____ is the most effective response when the parasite initially infects the hepatic cells
CMI
(T/F) abs are more protective when the parasite leaves the hepatic cells to infect the RBCs
True!
____ have the ability to survive within the phagocyte thus requiring a strong CMI to eliminate them
Leishmania
___ parasite elicits both humoral and cell-mediated response
Entamoeba
Helminths such as ____ and ____ are strictly extracellular pathogens
Schistosomes and Filaria
Th2 cells are important for development of the humoral response and inducing isotype switching to IgE via _____ and ____
IL-4 and IL-13
Adaptive response to parasites can be killed via _____
IgE mediated ADCC–> IgE binds to worm surface and eosinophils bind to IgE via Fc receptors causing degranulation
