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Micro/Immuno Part 2 > Immunity to Microbes > Flashcards

Flashcards in Immunity to Microbes Deck (29):

take home points

-only those organisms who successfully evade the immune response are successful pathogens
-primary adaptive immune response to bacteria is an antibody response. local is IgA and serum is IgG
-in most cases the microorganism is actually destroyed in a phagocytic cell
-only infected host cells are killed by CD8 cells
-specific immunity acts to enhance the uptake of microorganisms by phagocytic cells or to enhance the activity of phagocytic cells


innate immunity

-numerous non-specific barriers to infection exist that limit the entry of, or in the aid of rapid clearance of microoganisms:
pH barriers
phagocytes (with general receptors for bacteria-TLR)
-complement via alternate pathway (classical needs Ig)


virulence factors

-ability to survive the acid environment of the stomach as demonstrated by Salmonella typhosa
-production of spreading factors
-production of toxins that inhibit or kill immune cells
-the presence of an antiphagocytic capsule such as S pneumonia
-proteins like staph aureus protein A which binds and blocks the opsonizing action of IgG
-other antiphagocytic factors like M protein
-some bacteria are not flushed from the resp tract or the digestive tract due to their ability to attach to the epithelium


primary immune defense against bacteria




-prevent attachment to epithelium, mediated by secreted IgA
-trigger complement leading to increased opsonization or lysis
-bind to antiphagocytic M proteins or capsules, preventing the antiphagocytic activity and acting as an opsonin
-opsonized bacteria are not only taken up better but are also killed faster than are non-opsonized bacteria
-neutralize toxins
-neutralize spreading factors such as tissue damaging enzymes


facultative intracellular parasites

-ability to survive within the phagosome
-survive digestive enzymes of the phagolysosome or preventing the fusion of lysosomes with phagosomes
-examples are M TB and listeria monocytogenes


activated macrophages

-kill microorganisms much more efficiently
-result of specific T cell response
-TH1 helper repsonse
-sometimes need CD8 cells to kill infected macrophage to release the stowed bacteria for activated macrophages to eat it


immunity to listeria

-developed strain that will kill mice at high dose
-low dose will induce immunity
-these mice will be immune to the high dose of listeria
-phagocytosed by macrophages but not killed
-antibody increases the rate of phagocytosis but not the killing
-macrophages from the site of infection are able to kill-they are activated macrophages


listeria cont

-activated macrophages can kill many intracellular parasites (non-specific killing)
-long term immunity is specific
-immunity can be transferred from one animal to another will cells not serum
-the cells that transfer specific immunity are CD4+ T cells


cell mediated immunity

-specific immunity is a function of T cells
-non specific killing is a function of activated macrophages
-only live bacteria induced CMI, both live and dead produced antibody
-mechanism of antigen presentation is important in what response occurs
-TH1- cell TH2- antibody increases


two types of helper T cells

-TH1 stimulate CMI
-TH2 stimulate antibody production
-the way the dendritic cells present can influence response
-TH1 cells go to infected site to activate macrophages
-TH2 cells go the lymphoid tissues to activate B cells



-IL2, IFN gamma
-macrophage activation
-production of opsonizing antibodies
-TNF alpha



-IL 4,5, 10, 13
-general activation of B cells to make antobodies


IFN gamma and CD40 ligand

-kills intravesicular bacteria
-activates macrophages


Fas Ligand/LT

-kills chronically infected macrophages, releasing bacteria to be destroyed by healthy macrophages



-induces T cell proliferation


IL3 and GM CSF

-induces macrophage differentiation in the bone marrow


TNF a and LT

-activated endothelium to induce macrophage adhesion and exit from BV at site of infection



-causes macrophages to accumulate at site of infection


immune mechanisms involved in the clearance of parasites

1. T cell response is important in clearance and control
2. cytotoxic T cells are involved in limited manner-rarely kill parasites but may kill cells infected with the parasites
3. T cells activate macrophages that kill many different parasites
4. T cell dependent granulomata formation-interaction b/n activated macrophages that accumulate and release fibroblast growth factors-parasite walled off
5. T cells produce factors that causes the infiltration and increased production of eosinophils-can kill worms
6. T cells and B cells produce specific antibodies to parasite antigens
7. parasites have escape mechanisms


IgG and IgM

-able to kill some blood borne parasites-plasmodium
-complement mediated


antibodies and parasites

-neutralize some parasites by blocking receptor specific uptake into cells
-act as opsonin enhancing Fc and C3b mediated phagocytosis
-IgE-helminths-mast cells kill worms
-cellular toxicity from antibody can kill some organisms-macrophages, neutrophils, eosinophils and mast cells



-parasites can hide inside the hosts cells
-exist only in gut
-form cysts


avoidance of recognition

-vary cell surface antigen expression
-pick up host antigen



-t spiralis and leishmania can suppress host


immunity to viruses

-T cell mediated immunity important
-antibody prevents infection
-CTLs kill infected targets
-NK cells stimulated by T cells
-activated macrophages can kill infected cells


antibody and virus

-neutralizes virus
-binding of antibody to a portion of virus required for absorption, penetration, uncoating or replication
-steric hindrance
-localized IgA important to resp, GU, GU tracts
-in resp IgA is prime of antiviral
-may also lyse virions
-alone or with complement can increase rate of clearance by increasing rate of uptake by phagocytes
-can prevent but not likely to kill


CTLs and virus

-not always virus strain specific
-can immune against several strains of A with just one shot
-uses MHC class I



-alert other cells to protect themselves
-IFN a and b induce resistance to viral replication in all cells
-increase MHC class I expression and antigen presentation in all cells
-activate NK cells to kill virus infected cells