MCM 2-19 Immunity to Microorganisms 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
IgG
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
phagocytes
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
M-protein
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
- listeria lysin-o
- 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.
IL-2
t-cell proliferation, NK activation
IL12
important in stimulating TH1 response
IL10/IL4
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
two types of viruses
what do these require?
- Get into cell, and within 24 hours lyses the cell to release
- Virus gets in cell, over weeks and months the cell keeps pumping out virus, pushing It into cells near it
different types of immune response
dealing with viruses that enter cells and constantly bud off
Need to get CD8 cells to recognize infected cells, can do this on their own, but works best when CD4 is nearby to help.
TH1 cytokines include IL2 - necessary for stimulating CD8 to kill better. One case where THelper cells actually help a CD8 in addition to macrophages
describe the effects if IFN-1 (alpha and beta)
induces resistance to viral replication in all cells
increase MHCI expression and antigen presenttion in all cells
activate NK cells to kill virus-infected cells.
