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Chapter 24: The Immune System
NEW AIM: How does the body defend itself against MO’s?
Nonspecific (innate)
vs.
Specific (adaptive/acquired) Immunit
Chapter 24: The Immune System
NEW AIM: How does the body defend itself against MO’s?
I. Nonspecific (innate) vs. Specific (adaptive) Immunity
A. Nonspecific immunity
i. 1st line of defense
ii. Does not distinguish one pathogen from another
iii. Components
1. skin
- dead, stratified epithelium blocks MO’s
- acids secreted from skin glands
- Lysozyme
* Enzyme that breaks down bacterial cell wall
* Found in sweat, saliva, tears
Chapter 24: The Immune System
NEW AIM: How does the body defend itself against MO’s?
I. Nonspecific (innate) vs. Specific (adaptive) Immunity
A. Nonspecific immunity
i. 1st line of defense
ii. Does not distinguish one pathogen from another
iii. Components
1. skin
- desquamation of skin
* Your skin is stratified epithelium (many layers). Only the bottom layers are
alive and doing mitosis. The top (outer) layers are constantly falling off
along with anything attached to it like bacteria or viruses.
Chapter 24: The Immune System
NEW AIM: How does the body defend itself against MO’s?
I. Nonspecific vs. Specific Immunity
A. Nonspecific immunity
i. 1st line of defense
ii. Does not distinguish one pathogen from another
iii. Components
2. Beating cilia/mucus of respiratory system
3. Stomach acid
4. Hairs of nostrils
Chapter 24: The Immune System
NEW AIM: How does the body defend itself against MO’s?
I. Nonspecific vs. Specific Immunity
A. Nonspecific immunity
i. 1st line of defense
ii. Does not distinguish one pathogen from another
iii. Components
5. Nonspecific defense cells
- cells that confront microbes that get past skin,
digestive and resp. surfaces
a. Monocytes (become macrophages = big eaters) and neutrophils
•Collectively called phagocytes
(cyte = cell; phago = phagocytosis) – cells that phagocytose
b. Natural killer cells (do not confuse with killer T-cells)
* Attack viral infected body cells
Chapter 24: The Immune System
NEW AIM: How does the body defend itself against MO’s?
I. Nonspecific vs. Specific Immunity
A. Nonspecific immunity
iii. Components
6. Proteins
- interferons
The infected cell is done for and
will become a viral producing
factory. However, it will secrete a
protein called interferon, which will
warn neighboring cells that a virus
is in town.
Fig. 24.1
Chapter 24: The Immune System
NEW AIM: How does the body defend itself against MO’s?
I. Nonspecific vs. Specific Immunity
A. Nonspecific immunity
iii. Components
6. Proteins
- complement proteins
Complement proteins are always in your blood
in an inactive form. They are activated by
antibodies bound to a foreign cell (cancer cell,
bacterium, etc...). When activated, they make a
hole in the membrane causing the cell to lyse –
nutrients, organelles, etc... diffuse out.
Fig. 24.11
Chapter 24: The Immune System
NEW AIM: How does the body defend itself against MO’s?
I. Nonspecific vs. Specific Immunity
A. Nonspecific immunity
iii. Components
7. Inflammatory response (local)
- triggered by ANY tissue damage
Fig. 24.2
Chapter 24: The Immune System
NEW AIM: How does the body defend itself against MO’s?
I. Nonspecific vs. Specific Immunity
A. Nonspecific immunity
iii. Components
7. Inflammatory response (local)
histamine
Results in:
1. Rubor (redness) - due to vasodilation
2. Edema (swelling) – enhanced leakiness of blood vessesl
3. calor (warmth) – both due to enhances leakiness of blood vessels
Fig. 24.2
Chapter 24: The Immune System
NEW AIM: How does the body defend itself against MO’s?
I. Nonspecific vs. Specific Immunity
A. Nonspecific immunity
iii. Components
7. Inflammatory response (local)
- triggered by ANY tissue damage
- Rubor, edema, calor
- Coagulation cascade seals off area so bacteria
can’t get into the blood…
- Pus
The dead warriors (white blood cells and
bacteria) after the battle…
A pimple is a bacterial infection of a skin pore, pus is what is left after the battle.
Chapter 24: The Immune System
NEW AIM: How does the body defend itself against MO’s?
I. Nonspecific vs. Specific Immunity
A. Nonspecific immunity
iii. Components
8. Inflammatory response (systemic – entire system)
a. MO’s in blood and/or
b. toxins from bacteria in blood (recall exo- and endotoxins – ch27)
c. Body’s Response
- increase WBC count
- increase body temp. = fever (this is a normal response)
- triggered by toxins or chemicals released by WBC’s
- Higher temps stimulates phagocytes, gives your
WBC’s and advantage while at the same time
inhibits bacterial growth
Chapter 24: The Immune System
NEW AIM: How does the body defend itself against MO’s?
I. Nonspecific vs. Specific Immunity
A. Nonspecific immunity
iii. Components
8. Inflammatory response (systemic – entire system)
d. Septic shock (when the systemic response goes bad)
Septic shock is caused by cytokines (cell signaling molecules secreted by one cell to talk to another –
like hormones, but not secreted into blood) and by the toxins produced by some bacteria.
These substances cause the blood vessels to widen (vasodilate), which results in a drop in blood
pressure.
Consequently, blood flow to vital organs—particularly the kidneys and brain—is reduced. This
reduction in blood flow occurs despite the body's attempts to compensate by increasing both the heart
rate and the volume of blood pumped.
Eventually, the toxins and the increased work of pumping weaken the heart, resulting in a decreased
output of blood and even poorer blood flow to vital organs. The walls of the blood vessels may leak,
allowing fluid to escape from the bloodstream into tissues and causing swelling. Leakage and swelling
can develop in the lungs, causing difficulty breathing (respiratory distress).
Chapter 24: The Immune System
NEW AIM: How does the body defend itself against MO’s?
I. Nonspecific vs. Specific Immunity
A. Nonspecific immunity
iii. Components
9. Lymphatic system
a. Involved in both nonspecific and specific immunity
b. Lymph vessels, lymph nodes, tonsils and adenoids,
appendix, spleen, bone marrow, thymus
c. Lymph - fluid carried by vessels
- similar to IF, less O2 and nutrients
Chapter 24: The Immune System
NEW AIM: How does the body defend itself against MO’s?
I. Nonspecific vs. Specific Immunity
A. Nonspecific immunity
iii. Components
9. Lymphatic system
d. functions
i. return IF to circ. system
- vessels resemble veins
- valves, skeletal muscles propel lymph
- vessels are dead-ended
ii. fight infection
- in lymph nodes and other lymph organs
- lymph nodes
- packed with macrophages and lymphocytes
- lymphocytes involved in specific immunity
Chapter 24: The Immune System
NEW AIM: How does the body defend itself against MO’s?
I. Nonspecific vs. Specific Immunity
9. Lymphatic system
9. Lymphatic system
Fig. 24.3
Chapter 24: The Immune System
NEW AIM: How does the body defend itself against MO’s?
I. Nonspecific vs. Specific Immunity
A. Nonspecific immunity
iii. Components
9. Lymphatic system
Fig. 24.3
Chapter 24: The Immune System
NEW AIM: How does the body defend itself against MO’s?
I. Nonspecific vs. Specific Immunity
A. Nonspecific immunity
iii. Components
9. Lymphatic system
-Spleen
- destruction of old RBC’s
- rich in B and T cells for fighting
infection
- “large lymph node” for blood
- filters pathogens out of blood
Fig. 24.3
Chapter 24: The Immune System
NEW AIM: How does the body defend itself against MO’s?
I. Nonspecific vs. Specific Immunity
A. Nonspecific immunity
iii. Components
9. Lymphatic system
- Appendix
- Thought to be vestigial
- Possibly a shrunken cecum since
we no longer rely on hard to digest
plant material
- New studies suggest it harbors and
protects bacteria helpful to the colon.
- If an infection occurs in the colon, the
bacteria living there will be destroyed. Those
in the appendix can repopulate the colon.
- Contain WBC’s and may be
important in fighting infection
Fig. 24.3
Chapter 24: The Immune System
NEW AIM: How does the body defend itself against MO’s?
I. Nonspecific vs. Specific Immunity
Fig. 24.3
A. Nonspecific immunity
iii. Components
9. Lymphatic system
- Appendcitis
- Infection of the appendix
- Caused by an obstruction of the
opening to the appendix
- Fills with mucus and swells
- Blood flow disrupted, cells begin to
die (necrosis = dying cells), walls
begin to breakdown and if it breaks,
bacteria will enter your body cavity.
Appendectomy – removal of the appendix
Infected appendix
Chapter 24: The Immune System
NEW AIM: How does the body defend itself against MO’s?
I. Nonspecific vs. Specific Immunity
A. Nonspecific immunity
iii. Components
9. Lymphatic system
- Tonsils and Adenoids
- Trap bacteria/viruses as they
enter through nose and mouth
Fig. 24.3
Chapter 24: The Immune System
NEW AIM: How does the body defend itself against MO’s?
I. Nonspecific vs. Specific Immunity
B. Specific immunity (The Immune System)
i. More effective than nonspecific
ii. Used when nonspec. fails or in combination
iii. antigen
a. Foreign molecule that elicits immune response
b. Surface molecule of virus, bacteria, mold spores,
cancer cells, pollen, transplant, etc…
Why must it be a surface molecule?
The same reason that when a person is
wanted by the FBI they show a picture
of their face and not of their heart. The
surface of the cells is the part that other
cells and antibodies will “see”.
Chapter 24: The Immune System
NEW AIM: How does the body defend itself against MO’s?
I. Nonspecific vs. Specific Immunity
B. Specific immunity (The Immune System)
iv. Lymphocytes (B and T cells)
a. Spend time in lymph tissue
b. Produce the specific immune response
c. Originate in bone marrow
- 2 fates
1. Mature in bone marrow = B-cell
2. Leave bone marrow and circulate to
thymus, mature there and become a T-cell
Chapter 24: The Immune System
NEW AIM: How does the body defend itself against MO’s?
I. Nonspecific vs. Specific Immunity
B. Specific immunity (The Immune
System)
iv. Lymphocytes (B and T cells)
1. B cells elicit humoral immunity
Humoral implies humors or “fluids”. This response
will involve antibodies (proteins), which will be
dissolved in the fluids of the body – secretions like
saliva and breast milk, the blood plasma, interstitial
fluid, lymph fluid, etc… - to recognize foreign
substances (antigens)
2. T cells elicit Cell-Mediated immunity
In this case cells will be directly involved in
recognizing foreign substances (antigens)
Fig. 24.5
Chapter 24: The Immune System
AIM: How does the body defend itself against MO’s?
I. Nonspecific vs. Specific Immunity
B. Specific immunity (The Immune System)
v. Humoral immunity
a. B-cells make and secrete antibodies (a protein) into blood
b. We have millions of B-cells and each one produces a different antibody,
which will bind to a different antigen (one B-cell, one antigen).
(Epitope)
Antibody structure (quarternary structure)
Fig. 24.6
Chapter 24: The Immune System
AIM: How does the body defend itself against MO’s?
I. Nonspecific vs. Specific Immunity
B. Specific immunity (The Immune System)
v. Humoral immunity
a. B-cells make and secrete antibodies (a protein) into blood
b. We have million of B-cells and each one produces a different antibody,
which will bind to a different antigen (one B-cell, one antigen).
The antigenic determinant (epitope) is the
specific part of the antigen that the antibody
binds to via hydrogen/ionic/hydrophobic
interactions.
Fig. 24.6
Chapter 24: The Immune System
AIM: How does the body defend itself against MO’s?
I. Nonspecific vs. Specific Immunity
B. Specific immunity (The Immune System)
v. Humoral immunity
How can there be millions of B-cells each
expressing a unique antibody if we only
have 30,000 or so genes?? Wouldn’t we
need 1,000,000’s of genes, one for each
antibody?
Fig. 24.6
Chapter 24: The Immune System
AIM: How does the body defend itself against MO’s?
I. Nonspecific vs. Specific Immunity
B. Specific immunity (The Immune System)
v. Humoral immunity
How can there be millions of B-cells each
expressing a unique antibody if we only
have 30,000 or so genes?? Wouldn’t we
need 1,000,000’s of genes, one for each
antibody?
Fig. 24.6
Chapter 24: The Immune System
AIM: How does the body defend itself against MO’s?
I. Nonspecific vs. Specific Immunity
B. Specific immunity (The Immune System)
v. Humoral immunity
How can there be millions of B-cells each
expressing a unique antibody if we only
have 30,000 or so genes?? Wouldn’t we
need 1,000,000’s of genes, one for each
antibody?
Fig. 24.6
Chapter 24: The Immune System
AIM: How does the body defend itself against MO’s?
I. Nonspecific vs. Specific Immunity
B. Specific immunity (The Immune System)
v. Humoral immunity
How can there be millions of B-cells each
expressing a unique antibody if we only
have 30,000 or so genes?? Wouldn’t we
need 1,000,000’s of genes, one for each
antibody?
1. V(D)J recombination
There are many genes coding for each segment (V, D
or J) of the variable region. The genes will undergo
recombination in a given B-cell and a unique
combination of VDJ will result in both chains (light
chain doesn’t have a D segment).
Fig. 24.6
Chapter 24: The Immune System
AIM: How does the body defend itself against MO’s?
I. Nonspecific vs. Specific Immunity
B. Specific immunity (The Immune System)
v. Humoral immunity
How can there be millions of B-cells each
expressing a unique antibody if we only
have 30,000 or so genes?? Wouldn’t we
need 1,000,000’s of genes, one for each
antibody?
2. Somatic hypermutation
When a B-cell is activated it begins to rapidly divide.
The VDJ regions have an abnormally high rate of
mutation (1 nucleotide change per variable gene
[VDL] per division) during S-phase resulting in a
slight variations in all daughter cells – genetic
diversity followed by natural selection!!
Fig. 24.6
Chapter 24: The Immune System
AIM: How does the body defend itself against MO’s?
I. Nonspecific vs. Specific Immunity
B. Specific immunity (The Immune System)
Another name for an antibody is an
immunoglobulin or Ig for short.
There are five major types of
antibodies (IgG, IgM, IgA, IgD
and IgE – or G-MADE), each
has a slightly different function in
the body. For example:
IgG - found in the blood and interstitial fluid
and can cross the placenta giving immunity
to the fetus
IgA - found in external secretions like
saliva and breast milk.
Chapter 24: The Immune System
AIM: How does the body defend itself against MO’s?
I. Nonspecific vs. Specific Immunity
B. Specific immunity (The Immune System)
The five antibody (immunoglobulin)
types of mammals…
Chapter 24: The Immune System
AIM: How does the body defend itself against MO’s?
I. Nonspecific vs. Specific Immunity
B. Specific immunity (The Immune System)
v. Humoral immunity
a. B-cells make and secrete antibodies (a protein) into blood
b. We have million of B-cells and each one produces a different antibody,
which will bind to a different antigen (one B-cell, one antigen).
c. B-cells display the antibody they make (~100,000 of them) on their
surface as an antigen receptor and wait in the lymph system and spleen for an
antigen that will bind the antibody it makes…
Fig. 24.5
Chapter 24: The Immune System
NEW AIM: How does the body defend itself against MO’s?
I. Nonspecific vs. Specific Immunity
B. Specific immunity
(The Immune System) OVERVIEW
Memory T-cells are also made form Tcells activated by Helper T-cells. For a
future encounter with the same
antigen carrying pathogen.
Chapter 24: The Immune System
NEW AIM: How does the body defend itself against MO’s?
I. Nonspecific vs. Specific Immunity
B. Specific immunity (The Immune
System)
d. Clonal selection
v. Humoral immunity
- If the antigen does come along one
day, it will bind to the B-cell’s antibody
and activate the B-cell.
- The single activated B-cell will undergo
mitosis resulting in the formation of
plasma cells (antibody secreting cells)
and memory B cells…
(Activation actually requires a second signal
by a helper T-cell that we will discuss shortly)
- Why are plasma cells shown with a lot
of ER?
They are secreting incredible amounts of protein
(antibodies) and the ER/Golgi are required to do
this – recall endomembrane system.
Fig. 24.9
Now what do these antibodies do?
Chapter 24: The Immune System
NEW AIM: How does the body defend itself against MO’s?
I. Nonspecific vs. Specific Immunity
B. Specific immunity (The Immune
System)
v. Humoral immunity
Antibodies bind to antigens (surface
molecules), flagging them for phagocytosis
by phagocytes or activating complement.
Know all the terms like neutralization,
agglutination, precipitation…
What about those memory B-cells?
Fig. 24.11
http://catalog.nucleusinc.com/generateexhibit.php?ID=15529&ExhibitKeywordsRaw=&TL=1&A=2
Chapter 24: The Immune System
AIM: How does the body defend itself against MO’s?
Chapter 24: The Immune System
AIM: How does the body defend itself against MO’s?
I. Nonspecific vs. Specific Immunity
B. Specific immunity (The Immune
System)
v. Humoral immunity
1. Memory B-cells are soldiers that will wait in
reserve for the return of the same antigen.
2.These cells with memory T-cells are what gives you immunity.
STORY: You are infected with the virus Varicella zoster, which
causes chicken pox. A B-cell will recognize the virus somewhere
in your spleen or lymph nodes and be activated with the help of a
helper-T cell (discussed shortly). The B-cell will undergo mitosis
forming plasma and memory B-cells, which all make the same
antibody (it is mitosis so they are all ALMOST genetically
identical clones). Plasma cells will make and secrete antibodies
to fight the current virus, while many, many memory B-cells will
sit in lymph nodes and the spleen for the rest of your life possibly,
with the same antibody on their surface awaiting the return of the
virus/antigen. Initially there was only a handful of B-cells
Fig. 24.9
activated, the second response will activate 10,000’s!!
Chapter 24: The Immune System
AIM: How does the body defend itself against MO’s?
I. Nonspecific vs. Specific Immunity
B. Specific immunity (The Immune
System)
v. Humoral immunity
Why not make Memory B-cells for all 100+
million antibodies?
A. You do not have enough room in your lymph and spleen and
B. You would spend a huge amount of ATP to do this. You would
need to eat incredible amounts of food to maintain such a
system.
Fig. 24.9
Chapter 24: The Immune System
AIM: How does the body defend itself against MO’s?
I. Nonspecific vs. Specific Immunity
B. Specific immunity (The Immune
System)
vi. Cell-mediated immunity
a. B-cells fight the battle outside our cells, but what about when the
pathogen has gotten in like a virus that has turned your cell into a virus
producing factory?
- T-cells fight this one
b. We have million of T-cells in our lymph nodes and spleen and each one
produces a slightly different antigen receptor called a T-cell receptor (this is the
“antibody” of the T-cell although it well never secrete it).
Chapter 24: The Immune System
AIM: How does the body defend itself against MO’s?
I. Nonspecific vs. Specific Immunity
B. Specific immunity (The Immune
System)
vi. Cell-mediated immunity
c. STORY
1. It all starts when some kind microorganism
(microbe) gets engulfed by a macrophage (a mature
monocyte) of the innate immune system.
The macrophage needs to warn the specific immune
system as to what is going on!!
The phagocytosed microbe will be in a vesicle which
will fuse with a lysosome thereby partially digesting
the microbe.
2 and 3. The pieces of the microbe will then bind to
MHC-II receptors of the macrophage and be
displayed on the surface – the macrophage is now
called an Antigen Presenting Cell (APC).
Fig. 24.13
(MHC-II)
Chapter 24: The Immune System
AIM: How does the body defend itself against MO’s?
I. Nonspecific vs. Specific Immunity
B. Specific immunity (The Immune
System)
vi. Cell-mediated immunity
c. STORY
4. You have millions of Helper T-cells, each one
making a slightly different T-cell receptor (analogous
to B-cells each making a different antibody
receptor).
Fig. 24.13
(MHC-II)
A helper T-Cell (the same ones that HIV infects),
with a matching T-cell receptor to the displayed
antigen will bind to the antigen/MHC-II receptor of
the APC.
(MHC-II)
Chapter 24: The Immune System
AIM: How does the body defend itself against MO’s?
I. Nonspecific vs. Specific Immunity
B. Specific immunity (The Immune
System)
vi. Cell-mediated immunity
Interleukin-1 (IL-1)
Interleukin-2 (IL-2)
c. STORY
5. The APC will secrete interleukin-1,
a cytokine (a protein that acts as a
signal to instruct cells what to do),
which will bind to interleukin receptors
on the Helper T-Cell.
Interleukin:
Inter – between; leukos - white
A signal between white blood cells.
5
The combination of IL-1 and the MHC-II
complex activates the Helper T-Cell, and the
specific immune system has been notified!
Time to find out what the Helper T-Cell does…
Fig. 24.13
Chapter 24: The Immune System
AIM: How does the body defend itself against MO’s?
I. Nonspecific vs. Specific Immunity
B. Specific immunity (The Immune
System)
vi. Cell-mediated immunity
Interleukin-1 (IL-1)
Interleukin-2 (IL-2)
c. STORY
6. The helper T-cell will secrete interleukin2, also a cytokine, which will bind to
receptors on the T-cell itself, cytotoxic
(toxic to cells) T-cells, and B-cells, both of
which that have been partially activated by
the SAME antigen (remember earlier that I
said a B-cell would not fully activate with a
helper-T cell)
IL-2 stimulates the same Helper T-cell
that secreted it to undergo mitosis…
IL-2 will activate the B and cytotoxic T cells, which
have been partially activated already by the
SAME antigen – antigen binds to antibodies on Bcell surface or MHC-II on Cyto T-cell surface.
6
5
Cytotoxic T-Cell is also called a Killer T-Cell
Fig. 24.13
Chapter 24: The Immune System
AIM: How does the body defend itself against MO’s?
I. Nonspecific vs. Specific Immunity
B. Specific immunity (The Immune
System)
vi. Cell-mediated immunity
Interleukin-1 (IL-1)
Interleukin-2 (IL-2)
Fig. 24.13
Chapter 24: The Immune System
AIM: How does the body defend itself against MO’s?
I. Nonspecific vs. Specific Immunity
B. Specific immunity (The Immune
System)
vi. Cell-mediated immunity
Interleukin-1 (IL-1)
Interleukin-2 (IL-2)
c. STORY
**All of these lymphatic cells (B and T
cells) need two signals to be active:
1. The antigen
-An APC displays the antigen bounds to
MHC-II (the antigen/MHC-II complex),
which will bind to the T-celI receptor of a
Helper T-cell
- Binds directly to T-cell receptor of a
Cytotoxic T-cell that recognizes that
antigen.
- Binds directly to an antibody on the
surface of a B-cell.
6
5
Fig. 24.13
Chapter 24: The Immune System
AIM: How does the body defend itself against MO’s?
I. Nonspecific vs. Specific Immunity
B. Specific immunity (The Immune
System)
vi. Cell-mediated immunity
Interleukin-1 (IL-1)
Interleukin-2 (IL-2)
c. STORY
**All of these lymphatic cells (B and T
cells) need two signals to be active:
1. The antigen
What if the T-cell or B-cell does not have
an T-cell receptor or antibody, respectively,
that can bind to the antigen?
6
5
Nothing, that cell will not be selected.
Fig. 24.13
Chapter 24: The Immune System
AIM: How does the body defend itself against MO’s?
I. Nonspecific vs. Specific Immunity
B. Specific immunity (The Immune
System)
vi. Cell-mediated immunity
Interleukin-1 (IL-1)
Interleukin-2 (IL-2)
c. STORY
**All of these lymphatic cells (B and T
cells) need two signals to be active:
2. Interleukins
IL-1 from the APC will activate the partially
activated Helper T-cell.
IL-2 from the Helper T-cell will activate the
already partially activated Cytotoxic T-cells
and B-cells as well as itself
6
5
Now what will the activated Cytotoxic T-cells do?
Fig. 24.13
Chapter 24: The Immune System
AIM: How does the body defend itself against MO’s?
I. Nonspecific vs. Specific Immunity
B. Specific immunity (The Immune
System)
vi. Cell-mediated immunity
c. STORY
The cytotoxic T-cells will now bind to
infected cells displaying the SAME antigen
on MHC-I (MHC-ONE) receptors.
APC’s display antigen using MHC-II,
while infected cells use MHC-I.
Cytotoxic T-cells secrete the protein perforin onto
any cell with the proper MHC-I/antigen complex.
Perforin puts holes in the cell membrane causing
the cell to lyse...
Fig. 24.13
Chapter 24: The Immune System
NEW AIM: How does the body defend itself against MO’s?
I. Nonspecific vs. Specific Immunity
B. Specific immunity
(The Immune System) OVERVIEW
Memory T-cells are also made from Tcells activated by Helper T-cells. For a
future encounter with the same
antigen carrying pathogen.
Chapter 24: The Immune System
NEW AIM: How does the body defend itself against MO’s?
I. Nonspecific vs. Specific Immunity
B. Specific immunity
(The Immune System) OVERVIEW
Memory T-cells are also made from Tcells activated by Helper T-cells. For a
future encounter with the same
antigen carrying pathogen.
Chapter 24: The Immune System
NEW AIM: How does the body defend itself against MO’s?
I. Nonspecific vs. Specific Immunity
B. Specific immunity
(The Immune System) OVERVIEW
Recap: It all begins when a microbe is phagocytosed by a
macrophage or an antigen from the microbe binds to the
antibody receptor of a B-cell. The macrophage becomes an
APC when it displays pieces of the microbe attached to MHC-II
on its surface. The Helper T-cell with a T-cell receptor that
matches the antigen binds and it activated by interleukin-1
released by the APC. The Helper T will in turn secrete IL-2 and
activate itself to undergo mitosis as well as cytotoxic T-cells that
have also been partially activated by antigen binding to their Tcell receptors and B-cells that have already been partially
activated by antigen binding to their antibody receptors. The
cyto T-cells will undergo mitosis to make memory T-cells and
other cyto T-cells that will bind to the same antigen displayed on
MHC-I receptors of infected cells and lyse those cells using the
protein perforin, which puts holes in the membrane. B-cells will
undergo mitosis to make plasma cells and memory B-cells. The
plasma cells will secrete antibodies, which will bind to antigen
and mark objects with this antigen for death (phagocytosis by
macrophages). Memory B and T cells hang in the lymph nodes
and spleen awaiting the return of the antigen…
Chapter 24: The Immune System
NEW AIM: How does the body defend itself against MO’s?
I. Nonspecific vs. Specific Immunity
B. Specific immunity (The Immune
System)
vii. Memory cells
a. Memory B and T-cells are reservists for next time that specific
antigen shows up:
Primary immune response
The first time the lymphocytes see the antigen.
Antibodies are made, but relatively slowly due to
the small number of B-cells activated and only a
relatively small number of antibodies are made
compared to the second time the lymphocytes
see the antigen for the same reason.
Secondary immune response
The secondary response results upon reexposure to the antigen. You have millions of
memory B-cells. Most of them will be activated
and antibodies are made quickly and in large
number thanks to the large number of cells. You
do not get sick. It must be the same antigen. Any
mutation that changes the structure of the
antigen will not elicit the secondary response.
Fig. 24.8
Chapter 24: The Immune System
NEW AIM: How does the body defend itself against MO’s?
I. Nonspecific vs. Specific Immunity
B. Specific immunity (The Immune
System)
viii. Active vs. passive immunity
a. Active
1. Body produces own antibodies (plasma cells)
2. Permanent for the most part (memory cells)
- conveys immunity
b. Passive
1. Fetus gets antibodies from mom (doesn’t produce its own).
2. Antibody shots
Researchers are currently attempting to generate antibodies that will stick to cancer cells. How would this help
us?
3. Not permanent. Explain.
Protein are not highly stable like DNA and will only last a short amount of time before they lose their structure
(denature) and must be recycled. You are only protected for as long as the antibodies (immunoglobulins) last.
There is no way to replace them…
Chapter 24: The Immune System
NEW AIM: How does the body defend itself against MO’s?
I. Nonspecific vs. Specific Immunity
B. Specific immunity (The Immune
System)
viii. Active vs. passive immunity
a. Active
How can we use active immunity to our advantage?
Vaccines…train the immune system to recognize
antigens in a safe way…this can be done by injecting
bacterial/viral antigens into us…
Chapter 24: The Immune System
NEW AIM: How does the body defend itself against MO’s?
I. Nonspecific vs. Specific Immunity
B. Specific immunity (The Immune
System)
Smallpox
- infectious disease unique to humans,
- caused by either two virus variants: Variola major and Variola minor
- Localizes in small blood vessels of skin, mouth and throat.
- V. major - mortality rate of 30–35%.
- Long-term complications of V. major infection
- characteristic scars on face: occurred in 65-85% of survivors
- Blindness resulting from corneal ulceration and scarring: 2-5%
- Emerged about 10,000 BC
- killed ~400,000 Europeans each year during the 18th century
- responsible for a third of all blindness
- Between 20 and 60% of all those infected—and over 82% of infected children—died from
the disease
-20th century,
- 300–500 million deaths
- 1967, the World Health Organization (WHO) estimated that 15 million people contracted
the disease and that two million died in that year.
- 1979 - small pox is gone
Chapter 24: The Immune System
NEW AIM: How does the body defend itself against MO’s?
I. Nonspecific vs. Specific Immunity
B. Specific immunity (The Immune
System)
ix. Vaccines
a. First vaccine - small pox - 1797
1. Edward Jenner
2. Two related diseases: cow pox and small pox
3. Took pus from cowpox pustule and inserted it into an incision on a boy
4. Boy could not get small pox (he was immune)
Chapter 24: The Immune System
NEW AIM: How does the body defend itself against MO’s?
I. Nonspecific vs. Specific Immunity
B. Specific immunity (The Immune
System)
ix. Vaccines
b. Inject a harmless variant of disease causing microbe
1. Body responds to antigens
2. Memory cells produced
3. Immune system primed for the “real thing”
4. That’s easy…so where is the HIV vaccine?
HIV is a retrovirus. Viral particles that use reverse transcriptase and prone to
making more errors in their DNA that a virus using DNA polymerase. This results
in a quickly changing virus…the antigens change quicker than out immune
systems can keep up with. It is like a criminal that can shape-shift (change what
they look like…become anyone).
Chapter 24: The Immune System
NEW AIM: How does the body defend itself against MO’s?
I. Nonspecific vs. Specific Immunity
C. Overview
Non-specific
Specific
Chapter 24: The Immune System
NEW AIM: How does the body defend itself against MO’s?
I. Nonspecific vs. Specific Immunity
D. Autoimmune diseases
i. Immune system turns against the body
1. systemic lupus erythromatosus (lupus or SLE)
Butterfly rash
- Chronic autoimmune disease – lymphocytes attack connective tissue
- Causes inflammation
- Nine times more likely in women than men
- Unpredictable with periods of illness alternating with remission
- There is no cure, symptoms are treated
- Can be fatal, but fatalities are now rare with medical technology
- Precise cause is not known – genetic with environmental triggers
like UV light
Chapter 24: The Immune System
NEW AIM: How does the body defend itself against MO’s?
I. Nonspecific vs. Specific Immunity
D. Autoimmune diseases
i. Immune system turns against the body
2. Rheumatoid Arthritis
- Chronic systemic inflammatory disorder that mainly affects the joints
- 1% of worlds population affected by this, women 3X more likely than men
- Onset typically between 40 and 50 years of age
- Problems in addition to joints can occur like inflammation of lung tissue and
tissue surrounding the heart
- Treated of symptoms with physical therapy and anti-inflammatory drugs
- No cure, lifespan reduced 5 to 10 years (estimated)
- Precise cause is unknown
Chapter 24: The Immune System
NEW AIM: How does the body defend itself against MO’s?
I. Nonspecific vs. Specific Immunity
D. Autoimmune diseases
i. Immune system turns against the body
3. Insulin dependent (Type 1 early onset) diabetes
- Immune system attacks β (beta)-cells of the pancreas, which secrete insulin
- No insulin = no blood sugar regulation:
1. You eat a candy bar
2. Absorb monosaccharides into blood at jejunum
3. Blood sugar increases – sensed by proteins on the surface of beta cells in the pancreas
4. Beta cells secrete the hormone insulin (a protein) into the blood
5. Insulin circulates in the blood and binds to insulin receptors on the surface of muscle
and liver cells.
6. Muscle and liver cells respond by sending glucose transporters to the cell surface
causing the uptake of glucose in the blood, which will be stored as glycogen in the liver
and muscle cells.
- Treatment is insulin injections
Chapter 24: The Immune System
NEW AIM: How does the body defend itself against MO’s?
I. Nonspecific vs. Specific Immunity
D. Autoimmune diseases
i. Immune system turns against the body
4. Multiple sclerosis (MS)
- Immune system attacks schwann cells
- Schwann cells are nervous system cells that wrap around and insulate
neurons forming what is called the myelin sheath because the cells are
filled with myelin – a mixture of 80% lipid and 20% protein.
- Without these cells, electrical signals will leak and the signal will not make it to
where it needs to go…
- 5 to 10 years lifespan reduction, but suicide is a major concern
Chapter 24: The Immune System
NEW AIM: How does the body defend itself against MO’s?
I. Nonspecific vs. Specific Immunity
E. Immunodeficiency diseases
i. Lack one or more components of immune system
1. Severe combined immunodeficiency (SCID)
- Aka “Boy in the bubble syndrome”
- Disorder in which both B and T cells are
crippled due to defects in several possible
genes
- “Bubble” is a sterile (microbe-free) chamber
- The defective genes typically code for interleukin receptors.
- Most common treatment is bone marrow transplant
Chapter 24: The Immune System
NEW AIM: How does the body defend itself against MO’s?
I. Nonspecific vs. Specific Immunity
E. Immunodeficiency diseases
i. Lack one or more components of immune system
2. HIV – human immunodeficiency virus
- Reminder – infects and destroys CD4+ Helper T-cells
- No Helper T-cells, no activation of Cytotoxic Tcells and B-cells
- AIDS does not kill patient, a secondary infection
or cancer typically does due to a compromised
immune system.
- Treatment: Drug cocktails that inhibit multiple
enzymes at once to get the many variants and
avoid artificial selection due to rapid mutation of the
virus.
Chapter 24: The Immune System
NEW AIM: How does the body defend itself against MO’s?
I. Nonspecific vs. Specific Immunity
F. Allergies
i. Overreaction to environmental antigens (allergens)
Histamine
1. Allergen = surface protein of pollen, salivary proteins of dogs/cats, hair of
animals, etc…
2. Histamine binds cellular histamine receptors resulting in allergy symptoms
3. How do you think antihistamines work?
Chapter 24: The Immune System
NEW AIM: How does the body defend itself against MO’s?
I. Nonspecific vs. Specific Immunity
F. Allergies
ii. Anaphylactic shock
- hypersensitivity to an allergen (ex. Bee sting)
- sudden release of histamine by mast cells
- rapid dilation of blood vessels (swelling) / constriction of bronchioles
- rapid drop of blood pressure (shock)
- Emergency treatment = epinephrine (adrenaline)
- hormone that counters anaphylactic shock
- counters airway constriction (dilates airway)
- increases cardiac output to counter
drop in BP
Epi-pen = epinephrine pen
Chapter 24: The Immune System
NEW AIM: How does the body defend itself against MO’s?
I. Nonspecific vs. Specific Immunity