A&P 301 Immunology Notes:

The Immune System Function:

Protect the body from pathogens

Pathogen = anything that causes disease
Major pathogens: Bacteria, viruses, and fungus

The Immune System Types of Defenses:

Innate (Nonspecific) defenses

Adaptive (specific) defenses
Adaptive produces 2 things: 1) Produces antibodies, or 2) Produces cells that kill the
infected cells
Adaptive is SPECIFIC i.e. it will just kill the chickenpox virus, etc.
Innate = had is since birth
Innate system targets viruses more than bacteria, but not just specific viruses like the
adaptive/specific defense

Innate Defenses Mechanism:

First line of defense:

- Skin
- Mucosae
Second line of defense:
- Antimicrobial proteins
- Phagocytes
Know for the test!

Skin and Mucosae Mechanisms:

Acidity of skin secretions inhibit bacterial growth (acid mantle)

Stomach mucosa secretes acid and digestive proteins
Saliva contains lysozymes (Chews up bacteria)
Sticky mucus traps many microbes
You have nonpathologic strains of bacteria and fungi on your skin = normal skin flora
Bacteria and fungi are in competition with each other on the skin, which is why they
dont overgrow
Thrush in a child is d/t antibiotics messing with the competition of normal flora allowing
overgrowth
Streptococcus and Staphylococcus are the two major bacteria present on the skin
Candida is the major fungus on the skin
Skin is slightly acidic = does not favor growth of bacteria
Mucus is produced by the mucosal epithelium. Populates cavities open to the exterior
mouth, GI tract, etc.

Cells and Chemical Components:

Phagocytes
Natural Killer Cells (NK cells)
Inflammation
Antimicrobial Proteins
Fever

Phagocytes Cell Types:

Macrophages
- Monocytes name of cell IN the blood
- Macrophage name of cell after it LEAVES the blood
Neutrophils
Eosinophils
These are 3 of the 5 WBCs Lymphocytes and Basophils are not listed.
Keep in mind, these are NOT the only phagocytes in the body. Dendritic cells and B
lymphocytes are also phagocytic
WBCs DONT function in the blood the blood just carries them where they need to go
Their main function happens when they leave the blood

Phagocytes Mechanism of Action:

Particles are ingested and a phagosome is formed

The Phagosome is fused with a Lysosome to form a Phagolysome
Ingested particles are neutralized by a Respiratory burst
Lysosome is also a vesicle in cells that kills bacteria

Phagocytes Mechanism:

Adherence to be ingested the particle Must adhere to the Phagocyte

Adherence is more probable if the particle is coated with antibodies (called
Opsonization)
There are Lots of macrophages in the periphery, outside of the blood. They are rather
dormant
- An inactivated macrophage CAN still phagocytize the bacteria
- It then becomes Activated, once it eats the bacteria
- An Activated macrophage is More efficient than an inactivated/dormant macrophage
at phagocytizing
Adherence is an important principle - It HAS to be sticky or else the microbe cannot be
absorbed properly
Antibodies DO NOT kill microbes
Antibodies stick to microbes as a marker to other cells

Natural Killer Cells Description:

Lyse and kills cancer cells and virus infected cells

Active in blood and lymph
NONSPECIFC
NK cells are the FIRST lines of defense against Viruses
Unlike WBCs NK cells Are Active in the blood
NK cells are basically a lymphocyte but lymphocytes are part of the adaptive immune
system which is why it isnt categorized that way
NK is technically part of the Innate immune system
NK cells target viruses and cancer cells, they are ACTIVE in the blood

Natural Killer Cells Mechanism of Action:

Attack the target cells membrane by releasing Perforins

- Perforins disintegrates the membrane and nucleus
Is NOT phagocytic
Instead it Perforates the cell with perforins
Once it makes the hole via the peforins, it makes the cell rupture

Inflammatory Response Purpose:

Prevents the spread of damaging agents to nearby tissue

Disposes of cell debris and pathogens
Sets the stage for repair
Tissue does NOT heal unless there is an inflammatory response
Definition of inflammation: Increase in capillary permeability
Increase in permeability allows for fluid to go there and therefore allows the WBCs to
leave the blood and go to the site of inflammation
Inflammation does NOT equal infection

Inflammatory Response Triggers:

Physical trauma (surgery, etc.)

Intense heat (burns, etc.)
Irritating chemicals (acids and strong bases)
Infection
- Virus
- Fungus
- Bacteria
Is it better to have something acidic or basic on the skin? ACID, it flushes off quit easily.
Bases are more soapy and are harder to wash off.
What changes permeability of capillaries causing it to become inflamed? Chemical
messages by Cytokines
What changes causing the Neutrophils to stick to the blood vessels? Integrins and CAMs

Inflammatory Response Cardinal Signs:

Redness Erythema or Rubor (d/t increased permeability of capillaries)

Heat Calor (like Calorie)
Swelling Tumor
Pain Dolar
Impairment of function only considered by some
Remember for test!!

If it is inflammation: When you push down on skin it Blanches

If it is a bruise, broken blood vessels, etc.: When you push down on skin it stays Red

Inflammatory Response Cytokines:

Histamines
Kinins
Prostaglandins
Complement
Increased permeability is d/t chemicals released at the site of infection
Cytokine Any chemical produced that causes the immune response
IMPORTANT Concept: Purpose of phagocytizing cells in the wound
- 1) Destroy infectious substance
- 2) Causes immune response/inflammation

Inflammatory Response Results:

Chemicals INCREASE Permeability of local capillaries

Exudates (fluid containing clotting factors and antibodies) seep into the tissue space
Exudate = Plasma is exciting the blood with the clotting factors and antibodies
Exudates are especially seen in infections
You also see pus with an exudate
TRANSUDATE Plasma is just leaving by itself
Exudate causes LOCAL EDEMA
Protein fluid from the edema
- Dilutes harmful substances
- Brings oxygen and nutrients for repair
Edema fluid that has left and is trapped
Oxygen is extremely important
Any place in the body where there is loss of blood supply = RISK for Infection

Phagocyte Mobilization Components:

Extravasation
Leukocytosis
Margination
Diapedesis
Chemotaxis
Extraversion how neutrophils leaves blood and goes to site of infection

Phagocyte Mobilization Leukocytosis:

Leukocytosis-inducing factors promote rapid release of Neutrophils from Red Bone

Marrow
Leukocytosis = INCREASE in White cells
Leukopenia = DECREASE in White cells

Phagocyte Mobilization Components:

Extraversion is the term for the Entire process

- Margination
- Diapedesis
- Chemotaxis
You have Neutrophils in blood. Out of 5 types of WBCs, neutrophils are in the highest
concentration in the blood.
Neutrophils are the FIRST white blood cell to go the site of inflammation
Laminer flow opposite of which is turbulence
In non-inflamed capillaries the WBCs will just zip right on through
If capillaries get inflamed = WBCs in blood are going to come out toward the wall of the
capillary which is known as Margination
2 changes in inflammation response:
1) On the neutrophil there will be intagrent (sticky stuff)
2) And inflamed vessele will have CAM (cell adhesion molecule) which also makes it
sticky
-Integrin and CAM are the Velcro it gets the WBCs to stay

Phagocyte Mobilization Margination:

In inflamed areas capillary Endothelial cells sprout Cell Adhesion Molecules (CAM)
called Selectins that attract Neutrophils
The Neutrophils gather at the walls of the capillaries

Phagocytosis Mobilization Diapedesis:

Release of Neutrophils through the capillaries

The Neutrophils/WBCs leaving the capillaries change Shape. Looks round when its
leaving, but completely changes once it is outside of the capillary
Macrophages chew up bacteria and leaves a message for the Neutrophils to follow =
Chemotaxis

Phagocytosis Mobilization Chemotaxis:

Neutrophils release chemicals that attract other neutrophils initially

Monocytes then follow the neutrophils within 12 hours Monocytes become

Macrophages

Antimicrobial Proteins Types:

Interferon
Complement

Antimicrobial Proteins Interferon:

Produced by cells infected by a Virus

Causes uninfected (Healthy) cells to produce proteins that interfere with viral replication
Is NOT Virus specific
Interferon is produced by ANY cell that has a viral infection
It does NOT protect the cell that is infected, the immune system will kill it
The infected cell produces Interferon that travels to neighboring cells so viral
replication cannot happen
NOT specific = Under the INNATE immune system

Interferon Activates Macrophages and NK cells

Remember: NK cells are the FIRST line of defense against viruses
Also remember: Resting macrophage CAN phagocytize, but when activated it is more
efficient

Antimicrobial Proteins Complement Description:

Group of about 20 plasma proteins that circulate in an INACTIVE form

Provides the major mechanism for destroying foreign substances
Complement made up of a series of different proteins
All of these complement proteins have subunits, usually AB units, the AB units
separate and one will work on inflammation while the other Opsonization(?)
Plays a key role in destroying pathogens

Complement Activation Pathways:

Classical Pathway
Alternative Pathway

Complement Activation Classical Pathway:

Depends on antibodies attaching to invading organisms

Microorganism-antibody complex binds to Complement in a step called
Complement Fixation
What does the complement system do to a pathogen? Similar to NK cells, it perforates it.
There are two different pathways:
The microbe is covered by antibodies (MARKING it, not killing it) = Opsonization
Note: There are only certain antibodies that can attach to it: IgM and IgG are the
ONLY ones that bind to complement.

Complement Activation Alternative Pathway:

Other complement factors bind directly to the cell walls of the microbe
Know BOTH pathways for test!

Complement Activation Lysis:

Membrane attack complex (MAC) is inserted into the microbe by the complement
The MAC allows for an Influx of Calcium that destroys the microbe
They make the opening with the MAC
What kills the microbe? CALCIUM entering

Complement C-Reactive Protein:

Protein released by the liver that helps activate the common pathway
Used as a clinical marker for inflammation
There are 2 tests for inflammation:
ESR (erythrocyte sedimentation rate) takes tube of blood and RBCs will float to bottom
and plasma will go to the top.
- Looks at rate RBCs drop to bottom. If inflammation is present it takes the RBCs
longer to get to bottom
C-reactive protein also looks for coronary artery disease. Why?
- Coronary artery disease is a build up of plaque, in one spot (or multiple). Why did
cholesterol pick that particular spot? Because that spot is inflamed
Does Pill or Diet work better to control Cholesterol? Pill works better than diet to control
cholesterol because it reduces inflammation
Slide 32

Fever Mechanism:

Pyrogens released from Leukocytes produce fever

Fever causes the spleen and liver to sequester IRON and ZINC necessary for
microorganisms to reproduce
Fever produced by Pyrogens (pyro = fire)
How high can fever go? About 104 degrees
Fever makes you feel sick, muscles get extra tone (makes you fee fatigued, etc.) You
know antibiotics are working if it brings the fever down within 24-48 hrs.
Why is 104 important? If it gets higher brain damage is possible. The specific shapes of
proteins are known as Neutral State and are d/t different bonds.
- If temp gets high enough you damage those protein shapes and they become
denatured. The brain proteins get denatured
To bring fever down some use rubbing alcohol but it is NOT good. The alcohol can
become absorbed through the skin.
- ANY med you put on the skin can get into the blood, and too much rubbing alcohol
can cause toxicity

Fever doesnt really kill off the MO, it sequesters Iron and Zinc
Does Iron make a big difference in growth of bacteria?
- Its the same as having Lactorferrin like milk

Milk has Lactoferrin and it sequesters the Iron in milk and inhibits the growth of
bacteris
Febrile seizures (seizures in kids caused by fever)
- Febrile seizures are based on how fast there is a change in temperature.
- Doesnt necessarily mean they will have seizures as an adult
slide 33

Adaptive Defenses Categories:

Humoral immunity or antibody-mediated immunity = B cells and Helper T cells

Cellular or cell (or CMI/cell mediated immunity) - mediated immunity = Cytotoxic T
cells
The Adaptive immune system is Specific i.e. the B and T cells will ONLY fight the
chickenpox virus, etc.

Adaptive Defenses Antigens:

Complete antigens and Haptens

Antigenic determinants
Self-antigens
Antigens (something Foreign to the body) and Antibodies (protected by B cells)
PRINCIPLE of immune system: There are 2 things it has to do
1) Recognize something foreign (antigen)
2) Has to recognize SELF if it doesnt recognize self it will attack itself aka
Autoimmune disorders such as Rheumatoid Arthritis and Lupus/Systemic Lupus
Erythematosus (SLE)

Complete Antigens Functional Properties:

Immunogenicity able to stimulate proliferation o specific lymphocytes and antibodies

Reactivity ability to react with activated lymphocytes and antibodies
Immunogenicity STARTS the process
Reactivity carries out the process
Antigenic determinant sites differ from one bacteria to the next (all have different
shapes)
Every type of bacteria will have a different set of antigenic determinant sites

 T have an immune response the first time:

- Cytotoxic T cells and T cells look to see if the antigenic determinant is a close fit
- T cell receptor is specific to different shapes
- Nave T cell is one that hasnt been activated by the shape
slide 36

Haptens Functional Properties:

Also known as incomplete antigens

Are Small molecules
Have Reactivity but NOT Immunogenicity unless attached to a protein carrier
If you have an Incomplete antigen and antibody CAN still attach
A nave cell CANNOT be activated by it though, unless there is a Hapten present because
it wont recognize it

Antigenic Determinants Properities:

Antigens have specific spots that are Immunogenic known as Antigenic Determinant
Sites

Self-Antigens Properties:

Our cells have numerous antigenic determinants

Theses are recognized as Not being foreign to the body
T cell receptors (TCR) looks at ALL cells (i.e. our everyday cells)
Every nucleated cell has a flag pole or Major Histocompatability Complex (MHC),
when it becomes infected the original MHC flag comes down and a new flag
comes up saying it is Infected.

Self-Antigens Major Histocompatability Complex:

Proteins on the cell wall

MHC Class I on EVERY nucleated cell in the body
MHC Class II only on celled INVOLVED in the Immune Response
Cytotoxic T cell = kills infected cells, looks for any call in the body that is infected
Immune system KILLS infected cells, it does NOT fix them
Helper T cell = helps the B cell produce antibodies, it can only look at cells in the
immune system (immune cells)
MHC Class I Cytotoxic T cells look for this one
MHC Class II Helper T cells look at these
CONCEPT: T Cell Restriction or MHC restriction only Cytotoxic t cells can look at
MHC Class I , and Helper T cells can only look at MHC Class II

Major Histocompatibility Function:

In infected cells MHC binds to fragments of antigens so the cells are now Immunogenic
Infected cells display the infection on the MHC

HERE!
Humoral Immune Response Components:

Differentiation of B Cells
Immunological Memory
Active and Passive Humoral Immunity
Antibodies

Helper T cell helps the B cell, then the B cell produces antibodies

Differentiation of B Cells Fate of Clone Cells:

Most clone cells become plasma cells

Clone cells that do not become plasma cells remain as memory cells

Infinity maturation looking at antibodies they will produce. Pathogen has antigen
determinates, antibodies attach to ones that fit, once it fits it undergoes infinity
maturation where it produces ones that fit tighter.
o But this is not an intelligent process.
o Nave B cell undergoes infinity maturation.
Plasma cells produces antibodies
Memory cells similar role to nave B cells.
o Memory cell will become activated if it sees pathogen again.
If look at nave B cell and Memory B cell they will BOTH produce plasma cells
and memory cells
This is the primary and secondary immune response

Immunologic Memory Components:

Primary Immune Response

Secondary Immune Response
Secondary immune response have seen the pathogen before, will involve memory cells
Primary immune response has never seen the pathogen before, involves nave B cells

Immunologic Memory Primary Immune Response:

First exposure to a particular antigen

Response has a lag period of 3 to 6 days
Lag time represents time required for antigens to proliferate and B cells to turn into
plasma cells
3-6 days to undergo infinity maturation = lag time
This is TOO long, you will get the disease

Immunologic Memory Secondary Immune Response:

Occurs whenever reexposure occurs

**Faster, more prolonged, and more effective** than the primary response
Numbers are increased in 2 to 3 days
Secondary response antibodies bind with greater affinity
Blood levels remain high for weeks to months
2-3 days, meaning you will Not get the disease/infection
Secondary and Primary immune response - ACTIVE IMMUNITY. You are the person
producing the antibodies.
Infinity being able to bind tightly.
- Not only with antibodies
- Opsonization gave better infinity for phagocytic cells
Memory cells and antibodies in blood are constantly protecting you
Titer Tells you what the concentration of an antibody is
- Not just if you have them, but in what concentration
- If they bind they will sink to bottom.
- Titer is ratio, the larger the second number the more antibodies are present

Active Humoral Immunity Acquisition:

Naturally acquired during an actual illness

Artificially acquired by vaccination
Passive: When born, you are born with your mothers antibodies via the Placenta and
Colostrum. You did not make those antibodies, some else did = passive immunity.
Using serum from another persons blood = passive immunity
Passive immunity does NOT last, goes for 6 months at most. Then antibodies are gone.

Active immunity, you produced those antibodies yourself, you are now immune. Gives you
immunity.
Can get Active Immunity naturally or artificially
Rubella and Rubeola (hard measles, makes you light sensitive) = two types of measles

Active Humoral Immunity Vaccines:

May contain dead or attenuated (live but weakened) pathogens

Spare us from most of the symptoms of the actual disease
Provides functional antigenic determinants
Either Dead or Attenuated
Rubella is a live attenuated = potential to revert back and produce the disease
Anybody that acquires Rubella during pregnancy = possible birth defects
- Which is why we dont give Rubella vaccine to pregnant women

Passive Humoral Immunity Mechanism:

Antibodies are made by someone else

B cells are not challenged by antigens
A babys passive immunity lasts for about 6 months.
Which is why HCPs get concerned if a baby has a fever who is under 6 months.

Passive Humoral Immunity Types:

Natural passes through the placenta from mother to the fetus

Artificial given in serum such as gamma globulin
The tetanus vaccine takes too long to take effect, you gibe Gamma globulin (serum) if
youre really concerned

Antibodies Description:

Also called immunoglobulins (Ig)

Made of gamma globulins
Secreted by activated B cells or plasma cells
Antibodies bind to antigen
Antibody looks for antigenic determinates

 Antibody is actually adhering to antigen determinate

Antibody itself CANNOT kill antigen has to be other things involved such as
Opsonization (makes easier phagocytosis), and proteins from the complement system
-If pathogen is Opsonized, the complement system can come and destroy it.
- The MAC can then come in
Antigen binding site = binds to antigenic determinate
5 different classes of antibody are based on the tail

Antibodies Considerations:

Structure
Classes
Mechanism of Diversity
Targets and Function
Monoclonal Antibodies

Antibodies Basic Structure:

Consists of four looping polypeptides
- Heavy (H) chains
- Light (L) chains
The combination of the four makes an antibody monomer
Each chain forming an antibody has
- Variable (V) region
- Constant (C) region
Variable region is where the receptor is
It changes to fit the pathogen
Constant region does not change

Antibodies The Variables Region:

Has an antigen-binding site that fits a specific antigenic determinant

The variable region dictates what the antibody goes after

Antibodies The Constant Region:

Determines class

 Forms the stem of the antibody that makes up the effector region that dictates:
- What the antibody can bind to
- Antigen elimination
The constant region determines BIOLOGICAL ACTIVITY

Antibodies Classes:

Basic Y shaped structure is a monomer

Two linked together are a dimer
5 linked together is a pentamer

Antibodies Classes:
-

5 major classes
IgM
IgA
IgD
IgG
IgE
MADGE is the pneumonic

Antibody Classes IgM:

First antibody class released by plasma cells

Is the Pentamer
When the nieve B cell is first activated it produces the antibody IgM, but only for a short
time, then it produces IgG
Always link IgM and IgG in your mind
CANT cross the placenta, because as a Pentamer, it is too big

Antibody Classes IgG:

Most abundant of the Ig classes

Only Ig class that crosses the placenta
Involved in the secondary response
Is a Monomer
Involved in immune response.
It is the 2nd antibody produced in the Primary Immune Response
And the 1st antibody produced in a Secondary Immune Response

Antibody Classes IgA:

Called the secretory IgA

Found primarily in mucus and other secretions that bathe body surfaces (also in breast
milk)
Prevents antigens from entering the body
The antigen WILL enter the body, it just wont go unnoticed
IgA is variable from species to species

Antibody Classes IgD:

Always binds to the surface of B cells

Is therefore a B cell receptor only found on the surface of a B cell
It Doesnt float around like the others, it is a cell Marker (allows identification)

Antibody Classes IgE:

Involved is some allergic reactions

Cell markers for mast cells
Almost never found in the blood
WBC in body that contains Histamine = Basophils
Mast cell is responsible for allergies it is releases histamine.
Basophils will have the IgE sticking out of it. If pollen, etc. binds to two different IgE
receptors on the surface
- That is known as Cross linking, which is the single to the Mast cell to start releasing
Histamine
Pathogen vs allergen, whats in common & different:
BOTH invoke immune response (cells respond to them if covered in antibodies)
Pathogen = causes disease
Allergen = DOSESNT cause disease

Antibody Classes Complement:

Only IgM and IgG can fix complement

Meaning that Complement can Only bind to IgM and IgG

Antibodies Targets and Functions:

Antibodies only target antigens, they do not destroy them

Antibodies attached to antigens form an antigen-antibody (or immune) complexes
The Antigen-antibody complex works against you having the infection

Antibodies Targets and Functions:

Theses are the different things that antibody-antigen complexes do
Defensive mechanisms
- Complement fixation
- Neutralization
- Agglutination
- Precipitation
Neutralization = kind of like Opsonization, it completely coats pathogen with antibodies
but it cant attack
Agglutination and Precipitation are similar.
- Involves antigens attached to numerous antibodies that are attached together, until
there is a big clump of big antibodies and antigens.
Titer Looks for either Agglutination and Precipitation.
- Allows you to read it.
- Its what makes the RBCs heavy and go to bottom

Antibodies Monoclonal Antibodies:

Produced by descendants of a single cell and are pure antibody preparations for a specific
antigenic determinant

Used to diagnose:
- Monoclonal antibodies are really found when pt has Multiple Myeloma (Cancer)
- Pregnancy
- STDs
- Cancer
- Hepatitis
- Rabies

If you have Different variation of disease, one will attach and form secondary response,
other is new and will produce primary response
Different families of cells are known as Clones
See it come into play: Used to detect specific illnesses, but big thing they are known for
is *Multiple Myeloma* - one line of B cells is overproducing. Becomes so aggressive in
trying to push out antibodies that it attacks the bone

Cell-Mediated Immune Response T Cells:

Two major classes

- CD4
- CD8
- CD 4 Consists of Helper T cells (which combine with B cells for the production of
antibodies)
- CD8 Cytotoxic T Cells

T Cells CD4 Cells:

Also called T4 cells

Are helper T cells
Remember T cell can only bind with MHC II!

T Cells CD8 Cells:

Also called T8
Are cytotoxic T cells
Can only bind to MHC Class I!

CYTOTOXIC T Cells are the ONLY T cells capable of killing another cell

Cell-Mediated Immune Response Differentiation of T Cells:

Antigen recognition and MHC restriction

T cell activation
- Antigen binding
- Co-stimulation
Cytokines
There are 2 things a T cell must do: 1) Recognize self 2) Not overreact to self

Differentiation of T Cells Antigen Recognition:

T cells must have double recognition
- Antigens
- Self (MHC proteins of the body cells)
2 things it has to recognize
- 1) Antigens and,
- 2) Has to recognize self
This differentiation takes place in the Thalamus
Negative selection: Does not bind too tightly to self
Positive selection: Recognizes self
VERY few B cells make it to maturation
98% of T cells do NOT survive double recognition

Specific T Cell Roles Types:

Helper T Cells
Cytotoxic T Cells
Suppressor T Cells
Gamma Delta T Cells

Specific T Cell Roles Helper T Cells: Part of the Adaptive Immune System
aka Humoral Immunity

Stimulates proliferation of T cells and B cells that have been activated

Produce cytokines that recruit other leukocytes
Signal antibody formation to begin
Release cytokines that attract other types of white blood cells
Release cytokines that induce different subsets of T cells to differentiate
Cytokine leaves trail fro WBCs to follow = CHEMOTAXIS
Cytokines are also known as Chemokines. BUT while ALL Chemokines are Cytokines,
not all Cytokines are Chemokines
1st antibody produced during infection: IgM
The switches to IgG

Principle in Immunology: While the immune system is mounting an attack against the
pathogen it is also simultaneously preparing to wind it down

Specific T Cell Roles Cytotoxic T Cells:

Also called killer T cells

Only T cell that can attack and kill other cells directly
Roam the body circulating in and out of the blood
Main target is virus infected cells
Also attacks cells infected by certain intracellular bacteria (hard to treat because it gets
protection from the cell) or parasites, cancer cells, and foreign cells
Cytotoxic T cells are part of the Cell Mediated Immunity (CMI)!!
Still very specific

Specific T Cell Roles Suppressor T Cells:

Are regulatory cells

Releases cytokines that suppress B cells and other types of T cells
Winds down and stops the immune response
Tells B cells to STOP producing Antibodies
Start being made around the same time B cells and helper T cells are being activated

Specific T Cell Roles Gamma Delta T Cells:

Live in the intestine

Triggered into action when the TCRs bind to MICA receptors
Are more similar to natural killers
Where do you need the most protection? Anything that comes in contact with bacteria (so
in air, mucus membranes and stomach all have to be well protected)
Gamma Delta cells will go after ANY infected cell, unlike Cytotoxic and Helper T cells

Putting thing in perspective - Bacteria:

Antibiotics DONT differentiate between good and bad bacteria
-Acid mantle acid on skin
Immune cells underneath the skin: Macrophages and Dendritic cells
- Both of these cells are phagocytic!
Dendritic cell will pick up some bacteria and macrophages will too (phagocytize),
- What happens next? They will destroy it and take it back to blood and lymph nodes
- Cytokines drops off chemicals
- Cytokines will be trail for WBCs to follow = chemotaxis
-WBCs follow concentration gradient, go where the most cytokines are
1st blood cell that exits and goes to wound: Neutrophils
When neutrophil goes to wound, it will die there.
Are dendritic cells and macrophages done now that they have laid the chemical trail
- They are antigen-presenting cells. Takes part of microbe and present it on surface
- Then the T and B cells will look in lymph nodes to look and see whats being
displayed

Whats happening with a virus?

Cell 1st line of dense against virus (and cancer)? NK cells
Protein substrates that are released?
- Perforins which pops hole in membrane
What determines if you get the virus or not?
- Antigen load (infectious dose) determines if youll get sick or not.
- Virulence also plays a role
Macrophages and Dendritic cells will still phagocytize a virus
Difference between Innate and adaptive immunity
If innate immune system completely clairs out pathogen, then you will NOT gain
immunity
If innate Doesent clear out the entire load of pathogens, and you get the disease then the
adaptive immune system takes over and you get immunity.

We cannot have an adaptive response, without the innate immune

system working first!!!