immune system test Flashcards
2 parts of immune response
innate and adaptive
the innate immune system is
nonspecific, 2 parts
part 1 of innate immune system
physical/chemical barriers to keep contaminants out
part 2 of innate immune system
responses like macrophages, inflammation, and fever to keep microbes at bay
adaptive immune response
how the body learns to specifically target and eliminate contaminants
skin
(normally) solid barrier that stops bacteria from getting inside inside the body
the outer layer of the skin is coated in
protein keratin
function of keratin in the skin
works with other lipids and proteins to form a tight seal separating inside from out
The outer cells of the skin
is continuously shedding , this is called desquamstion
desquamation takes
attached microbes with them
the skin secretes waxy, oily
sebum
sebum gives the skin a pH of about what
5.5
pH of sebum is
acidic compared to body’s 7.4
change in pH due to sebum can cause
denature enzymes in bacteria, slows their function
95% of infections from
begin in the mucous membranes
5% of infections result from
vector bites
Other pH barriers to microbes
saliva
stomach
vagina
saliva pH
roughly neutral (7)
pH of stomach after a meal
2
pH of stomach at rest
3.5
inside of vagina pH
4
what are the OTHER physical barriers to microbes
mucus, urinations, defectation, vomitting, tears, hairs and cilia
where is MUCUS found
airway, esophagus, stomach, intestines, cervix (females)
how does mucus affect microbes
microbes stick to it and are broken down by protein and/or expelled from the body
what washes microbes out of the body
urination, defcetation, vomiting and tears
hairs in the nose and cilia in the windpipe can….
stop microbes from entering the lungs
because of cilia…. bacteria are pushed
up and away from the lungs through the mucociliary elevator
if a particle is detected in the airway
extremely sensitive nerves in the airway will force a cough reflex
lysozyme (a chemical barrier)
lysozyme is an enzyme in tears, mucus, breast milk, saliva
lysozyme function
breaks apart peptidoglycan, kills bacteria
what is peptidoglycan
main component of bacterial cell walls,
normal flora
bacteria living on it in a mutualistic relationship
instead of harming the body………
many benefits
benefits of normal flora
- nutrients that the body can’t normally provide (B12)
- competition for space and nutrients,
- create compounds that kill other bacteria
- modify the pH of an area to make it inhospitable to other bacteria
competition for space and nutrients causes
makes it hard for bad bacteria to survive
how much human cells in the body
10^13
how much symbiotic bacteria in the human body
10^14
first step of phagocytosis
- chemotaxis and adherence of microbes to phagocyte
second step of phagocytosis
- ingestion of microbe by phagocytosis
step 3 phagocytosis
formation of a phagosome
step 4 phagocytosis
fusion of the phagosome with a lysosome to form a phagolysosome
step 5 phagocytosis
digestion of ingested microbe by enzymes
step 6 phagocytosis
formation of residual body containing indigestible material
step 7 phagocytosis
discharge of waste materials
phagocytes
white blood cells that eat and destroy foreign contaminants through phagocytosis
types of phagocytes
neutrophils
macrophages
dendritic cells
neutrophils function
eat bacteria
macrophages function *
eat everything that dosen’t have a proper ID
dendritic cells function*
eat surroundings that show PAMPS
macrophages and dendritic cells
present digested guts to surrounding cells, especially T cells
what is PAMPs
micro-associated patterns
PAMPs
pathogen-associated molecular patterns
peptidoglycan (PAMPs)
main bacterial cell wall component, gram positive
peptidoglycan chemical surrounds
membranes of many bacteria
if a bacterial membrane contains a thick layer of peptidoglycan
gram positive
why is something gram positive
turns purple when dyed w/ Gram method
if it does NOT turn purple hen dyed with the gram method
gram negative… turns pink instead
LPS (PAMPs)
main bacterial membrane component, gram negative
LPS
lipopolysaccharides
what are LPS
long chains of sugars that attach to membranes of gram-negative bacteria with thin peptidoglycan layer
Flagellin (PAMPs)
a protein found in bacterial flagella
many bacteria have a flagellum
to help them move through the body
many flagellum
flagella
main protein in flagella
flagellin, is a PAMP
Double stranded RNA (PAMPs)
found in viruses
glucans (PAMPs)
major component of fungal cell walls
PRRs
Pattern Protein Receptors
where are PRRs found
they are proteins found on the plasma membrane of macrophages
job of PRRs
recognize PAMPs
2 main types of PRRs;
Phagocytosis receptors
TLRS
Phagocytosis receptors
binding to a PAMP causes the onset of phagocytosis..
phagocytosis receptors are only found in
phagocytes
TLRs
toll-like receptors
TLRs function
bidning to PAMP causes the activation of genes coding for cytokines
what are cytokines
signalling proteins
where are TLRs found
phagocytes, epithelial cells and MORE
there are many kinds of TLRs that each
recognize specific microbial compoents
each TLRs trigger the
release of some cytokines
cytokines are….
small proteins produced by various white blood cells
cytokines are produced in response to
PAMP binding to a TLR
cytokines can be
autocrine
paracrine
endocrine
autocrine (cytokine)
meaning they act on the red blood cell that secrets them
paracrine (cytokine)
they act on nearby cells
endocrine (cytokine)
travel longs distances in the body
3 things tat cytokines cause to happen
- vasodilation of blood vessels
- upregulation or downregulation of genes
- white blood cell hematopoiesis
3 OTHER THINGS that cytokines can cause
- production of antobodies
- apoptosis
- inhibition of viral replication
chemokines
are a type of cytokine, attract molecules through chemical signals
two categories of chemokines
homeostatic
inflammatory
homeostatic chemokines
attract various types of white blood cells to the area and invoke diapedesis
what is diapedesis
jumping through the walls of a vessel into infected tissue
what is chemically attracted to chemokines
white blood cells
inflammatory chemokines
initiate the inflammatory response by causing vasodilation
vasodilation caused by inflammatory chemokines….
leads to more blood, and in turn more white blood cells in the area
inflammation can be
acute or chronic
acute
quick onset
chronic
long term
signs of inflammation
redness, heat, swelling, pain
positive feedback loop of cytokines
cytokines made to recruit WBS, which release cytokines to recruit even more WBCs
the positive feedback loop of cytokines is supposed to be
localized and shut off at a certain point
if an infection gets too big
the body does not to shut down the cytokines»_space;> CYTOKINE SToRM
result of a cytokine storm
widespread inflammation
widespread inflammation from a cytokine storm can cause
ARDS»> DEATH??!??!?
ARDS
acute respiratory distress syndrome
cytokine storm can also cause
severe damage to blood vessels when they dilate too much
damage to blood vessel can lead to
blood spilling the extracellular space
blood spilling the extracellular space causes
reddish splotches on the skin (petichaie LOOK It up), shock
fever invoked
by pyrogen
pyrogens can be classified as
endogenous or exogenous
exogenous pyrogens
come from outside and bind to PRRs to trigger the release of endogenous pyrogens
example fo exogenous pyrogen
LPS . (lipopolysaccharide)
endogenous pyrogens
are cytokines made by macrophages in RESPONSE to exogenous pyrogens
examples of endogenous pyrogens
interleukin-1 (IL-1) and interleukin-6 (IL-6)
endogenous pyrogens travel
to the hypothalamus in the brain….. send hormonal signals across the body to increase temperature
fevers help stop
bacterial growth (deature?!)
fevers increase
ability of certain macrophages to do their jobs by altering their membrane fluidity.
how does inflammation cause its symptoms
- capillary widening
- increased capillary permeability
- attraction of white blood cells
- systemic response
capillary widening can cause
increased blood flow
increased capillary permeability can cause
release of fluid
attraction of white blood cells can cause
migration of WBCS to injury
systemic responses can cause
fever and proliferation of white blood blood cells
antibodies
small y shaped proteins
antibodies structure
the same except the two tips of the Y
two tips of the Y structure
heavily variable , infinite shapes, almsot every molecule
stem of the Y of antibodies
Fc region
branches of the Y
FA=ab regions
antigens
the shreds resulting from pathogens being broken down by phagocytes
how are antigens sensed
by antigen binding sites on antibodies
another name for antibodies
immunoglobulins
Ig
immunoglobulins
5 types of immunoglobulins
IgG*, IgM, IgD, IgA, and IgE.
most common Ig
IgG
B cells
white blood cells who create antibodies
Each B cell..
creates just one specific antibody
how do B cells create antibodies
through V(D)J recombination
After a B cell’s antibody recognized a pathogen and has treated the body
B cell becomes a memory B cell
what do memory B cells do after becoming one?
travel to lymph node and lies dormant
memory B cells lie dormant in lymph nodes until
the same antigen is spotted
what happens when the same antigen (already been treated by a memory B cell) is seen again
dormant B cells rapidly creates antibodies (MUCH FASTER)»_space;»»»
When dormant B cells rapidly create antibodies… the body
bodies is quickly cured .. often before sickness is felt
B cell phenomenon is basis for
vaccination
T cells
type of white blood cell produced in the thymus
thymus location
JUST SUPERIOR TO THE HEART
Like B cells, T cells are also
antigen-specific
TCRs
T cell receptors
t cell receptors
special receptors on the membranes of T cells
what do TCRs do
look for digested pieces of stuff that macrophages and dendritic cells have broken apart during phagocytosis
if TCRs see “bad stuff”»_space;> 3 reactions for what 3 cell types
cytotoxic T cells,
helper T cells
regulatory T cells
cytotoxic T cells
hunt down and kill cells that contain a certain anitgen
helper T cells
begin producing cytokines
cytokines released by helper T cells….
will attract B cells, cytotoxic T cells and macrophages, and will cause white blood cell hematopoiesis
regulatory T cells
shut down other T cells at the end of an immune response
smaller sub-region of an antigen
epitopes
what are epitopes recognized by
paratopes on antigens
most pathogens
have many epitopes, can be recognized by many antibodies
4 MAIN METHODS FOR ANTIBODIES FIGHTING PATHOGENS
Neutralization
Agglutination
Precipitation
Complement Activation
when the Fab region(s) of an antibody bind to the antigen…
Fc ragion dangles off
many phagocytes have special….
special receptors called opsonin receptors…
opsonin receptors
increase the chemical attraction between themselves and dangling Fc regions
main idea of opsonin receptors
makes marked antigens look more delicious to phagocytes
neutralization
antibody physically blocks the antigen from having its effect
example of antibody neutralization
Corynebacterium diphtheriae
Corynebacterium diphtheriae
bacteria that secretes small protein diphtheria toxin
diphtheria can…
ENTER CELLS AND BREAK THE eEF-2 protein
eEF-2 protein
vital part of protein synthesis in human cells
antibody for diptheria
blocks diphtheria from binding to receptors and entering the cell
so if dipheria toxin is neutralized by the antibody
eEF-2 is never turned off
agglutination
the clumping together of molecules
in agglutination some antibodies will cause
bacteria or mother molecules to stick together in large groups
when agglutination happens it makes it
easier for phagocytes to engulf them after opsonization
agglutination also plays a major role in
blood types
blood types
A, B, AB, or O
Type A blood
have A antigen on RBCs (and B antibody in blood
Type B blood
have B antigen on RBCs (and A antibody in blood)
Type AB blood
have A and B antigen on RBCs (no antibodies in blood)
Type O blood
have neither A or B antigen on RBCs (both antibodies in blood)
when would a blood transfusion go bad
a person gains a transfusion of blood with an antigen they have antibodies fo
if a person gains a transfusion of blood with an antigen they have antibodies for
the antibodies will cause RBCs to agglutinate and then lyse.
if red blood cells agglutinate then lyse
free hemoglobin clogs the kidneys»_space; shut down
some antigens, but usually………..
usually harmful pieces of a virus, are solube
soluble antigens
hide in the body by dissolving in serum
what can antibodies to to fight the antigens that dissolve to hide
bind to them and force them out of solution to form a solid precipitate
when antibodies bind to antigens to form a solid precipitate
makes them easier targets for phagocytosis
in order for precipitaion to work
Roughly equal part of antigen and antibody
precipitation is often coupled with
agglutination
complement pathway is cool because…
shared component of adaptive and innate immune systems
complement pathway is turned on by
presence of PAMPS or signal from antigen-antibody complexes
_______ released because of PAMPS or antigen-antibody complexes
cytokines, lead to a cascade that makes many different proteins together
cytokines and cascade that makes many different proteins together
form a giant pore in a pathogen membrane» KILLS it
autimmune disease
are a broad class of diseases where the body “attacks itself
what happens in an autoimmune disease
antibodies in the body mistake “self” cells for “nonself” cells and begin attacking them.
what things to autoimmune diseases cause
tissue damage
increased tissue growth
altered tissue function
primary immune response
first time the body sees an infection…. takes while to gather the troops
secondary immune response
each subsequent time the body sees an infection… faster and stronger reaction
vaccinations
expose the body to a pathogen without getting youu sick
what are the three ways a bacterium or virus is prepared for a vaccine
attenuated
killed/inactivated
subunit
attenuated vaccine
bacterium/virus is alive…. genetically modified so that bad genes are removed
killed/inactivated vaccine
bacterium/virus is grown in lab then killed by heat or formaldehyde…. dead specimen injected
subunit vaccine
bacterium/virus grown in lab… … …only one part (a single epitope) is placed into vaccine and injected
what parts are usually injected in a subunit vaccine
capsid in viruses, membrane or wall component in bacteria
examples of attenuated vaccination
MMR, Measles, Mumps, Rubella
examples of killed/inactivated vaccination
Polio
example of subunit
hep. B
pros of attenuated vaccination
- small dose
- usually no booster
- giver STRONGEST IMMUNITY
cons attenuated vaccination
- must be refrigerated
- small risk of mutation to regain pathogenicity
- may cause adverse reaction
pros of killed/inactivated vaccination
- no risk of mutation to regain pathogenicity
- does not need to be refrigerated
cons of killed/inactivated vaccination
- much larger doses required -often needs booster shots
- may cause adveerse reaction
which is more likely to cause adverse reaction: killed or attentuated
attenuated
pros of subunit vaccination
- no risk of mutation to regain pathogenicity
- does not need to be refrigerated
- not likely to overwhelm immune system and cause adverse reaction
cons of subunit vaccination
- gives “weakest” immunity b
- much larger doses required
- often requires boosters
why does subunit vaccination give the weakest immunity
only one or a few epitopes recognized
what disease did we eradicate
small pox
what type of immunity do vaccines provide
active (artificial)
what is the basis of active immunity
causes your body to make memory B cells that recognie
antigens and spring into action the next time encountered
active immunity generally lasts….
for life
when is passive immunity usually used
time-sensitive cases
examples of uses for passive immunity
snakebites… tetanus infection for unimmunized …… patient w a weakened immune system
what is the basis for passive immunity
injecting neutralizing antibodies harvested froma different host into the patient
passive immunity generally lasts…
days to months (TEMPORARY)
active natural immunity
patient catches disease, develops own antibodies and build up memory B cells that will fight it the next tuime
active artificial immunity
patient receives (attenuated, dead, subunit) vaccine, gains memory B cells without actually fighting it
passive natural immunity
infant patient drinks breastmilk, receives mother’s antibodies, temporary protection form many disease
passive artificial immunity
patient receives injection of antibodies from donor organisms that neutralize antigens and give temporary immunity.
what are often donors for passive artificial immunity
horses, pigs etc
