MCM 2-19 Immunity to Microorganisms Flashcards Preview

MSI Unit II > MCM 2-19 Immunity to Microorganisms > Flashcards

Flashcards in MCM 2-19 Immunity to Microorganisms Deck (33)
Loading flashcards...

which organisms will be successful pathogens?

only those organisms that can successfully evade the immune response


primary adaptive response to bacteria is...

the primary local immune response is

the serum antibody response is mostly

antibody response

an IgA response



in most cases the microorganism is actually destroyed in a

phagolytic cell


only infected host cells are killed by

CD8+ cells


specific immunity acts to enhance the uptake of microorganisms by

phagocytotic cells or to enhance the activity of phagocytotic cells


innate immunity protects us against..

99% of bacteria. only the smallest percentage get in and cause disease


you can't live without


you can live without B cells and T-cell


Rule #1: most bacteria die within

a phagocyte


how does complement recognize microbial surfaces?

complement doesnt specifically recognize microbial surfaces, its the fact that our own cells have inhibitors which are lacking on microbial surfaces


spreading factors

enzymes on skin and tissue that break down collagen connection, let bacteria in


what do most toxins do

most toxins (not including tetanus) kill immune cells. The hemolytic properties of bacteria are due to toxins that kill blood cells both red and white


Protein A

found in staph aureus, binds to and blocks opsonization action of IgG



an antiphagocytotic factor


epithelium attatchment

allows bacteria like cholera/mycobacteria not to get washed away


activities of antibody

IgA prevents attatchment to epithelium, doesn't allow bacteria to stick, gets washed away by mucus or in the digestive tract

triggers complement leading to increased opsonization/lysis

binding to antiphagocytotic Mpreoteins or capsules, preventing antiphagocytotitc activity and acting as an opsonin (for phag and NK cells)

opsonized bacteria are taken up better and killed faster

neutralize toxins before they can harm immune cells

neutralize spreading factors as tissue damaging enzymes


2 main facultative intracellular parasites

mycobacterium tuberculosis (MTB)
listeria monocytogenes (LM)


describe activity of listeria

gets inside phagosome, detects environment (slightly acidic) and produces 2 enzymes
1. listeria lysin-o
2. phospholipase C

these two enzymes destroy the phagosome, listeria gets into the cytoplasm of the cell. In cytoplasm, forms ACT-A that depolymerizes actin and can shoot itself into neighboring cells


process of listeria immunity

developed listeria strain that would kill mice when high dose of bacteria injected

low dose will induce short-term growth but will give immunity

these mice will not be immune to high dose of listeria


molecular level of listeria immunity

initially listeria phag but not killed
added antibody to listeria, phag faster but not killed

take macrophages from site of infection are able to kill - these are activated macrophages with heightened and new activities

could kill everything better, but the immunity was not humoral the immunity was cellular.


describe activated macrophages

able to kill better, kill everything better. they were non-specific at killing just like regular macrophages are non specific


what passed immunity from one mouse to the other?

CD4+ t-cells, not serum.


live listeria vs dead listeria response

live - macrophages
dead- antibodies

it must be the presenting cells are making the distinction. the T-cells see antigen on surface of phagocyte. something about APC was detecting if the listeria was growing inside of it or not, causing a shift in influencing t-cells to become TH2 or TH1. The t-cell was making a choice based on how antigen was prseneted and what cofactors were being expressed.


Two types of Helper T-cells

helper T-cells are CD4+

TH1 stimulate cell mediated immunity
TH2 stimulate antibody production


Effect of TH1 vs TH2

TH1 - macrophage activation, some b-cell activation, production of IL2 and IFN gamma. production of opsonizing antibodies such as IgG1. TH1 will see macrophage and give signals (IFN-gamma and CD40 ligand) to macrophage to activate it

TH2 - b-cells will make lots of antibodies, produce IL4 and IL5


dealing with infected macrophages

One of the things that happens when you have listeria infection, and the macrophage is filled
With listeria in its cytoplasm. You can activate the macrophage all you want, but the cytoplasm is not where bacteria gets killed. Cytoplasm is safe, phagosome is wehre bacteria get killed. Nothing about cytoplasm that is toxic. So what you have to do with infected cell is kill it to release bacteria so they can be taken up by a now healthy activated macrophage which can kill it.

Even cd8 cells killing infected macrophage is part of response to listeria.



t-cell proliferation, NK activation



important in stimulating TH1 response



important in stimulating TH2 Response


necessary signals for TH_ cell to stimulate a b cell

TH2 stimulate B-cells

-IL4, 5,6 along with CD40


____ are critical for immunity to parasites

T cells. Activation of macrophages, no direct killing

Decks in MSI Unit II Class (46):