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Transcript
Immune System
Animals have various means of defense against
pathogens—agents that cause disease.
Defense systems are based on the recognition of
self (one’s own) and nonself (foreign) molecules.
Two general types of defense mechanisms:
Nonspecific defenses: protect against anything
& everything (aka Innate)
Specific defenses: aimed at specific pathogens
(aka Adaptive)
Non-Specific Immunity
Barriers: skin
mucous membranes
cilia & mucus
normal flora
phagocytosis by macrophages
inflammation
Blood
plasma + RBCs + WBCs + platelets
transport for both non-specific and specific
Lymph
derived from blood;
returns fluid from tissue
to circulation
nodes- cells of the
immune system
reside here and
check fluid for pathogens
Red and white blood cells originate from
pluripotent stem cells in the bone marrow.
These cells constantly divide and can
differentiate into a variety of blood cells.
http://www.youtube.com/watch?v=I_xh-bkiv_c&feature=related
Specific Immunity
Antibodies are proteins that bind to substances
identified as nonself. Secreted by B cells.
T cell receptors are integral membrane proteins,
recognize and bind nonself molecules on other
cells.
Major histocompatibility complex (MHC): on the
surface of most mammalian cells. They are selfidentifying labels.
Antigens: protein or part of protein-flag = not me
T cell receptors and antibodies bind to
specific nonself molecules (antigens).
Specific sites on the antigens are called
antigenic determinants or epitopes.
The specific immune system has four key
traits:
• Specificity
• Diversity—response to a wide variety of
pathogens
• Ability to distinguish self from nonself
• Memory
Humoral vs. Cellular Response
Antibody reacts to Antigen in
blood, lymph & tissue fluids
Triggers B cells to clone itself
plasma cells make Antibody
that binds to pathogen
memory cells-perpetuate
clone & reduce response
time at 2nd exposure
T cell receptor recognizes
Antigen + MHC (me signal)
Triggers T cells to clone itself
T-cytotoxic –destroys cells
with MHC1 + antigen
T-helper-alerted by MHC2 +
antigen-stimulates B cells to
proliferate
T-suppressor-turn off
response
Figure 24.7A
Primary immune response
Secondary immune response
2
1 B cells with
different
antigen
receptors
Antigen
molecules
Antigen
receptor
on the cell
surface
Antibody
molecules
3 First exposure
to the antigen
Cell activation:
growth, division,
and differentiation
Antigen
molecules
Antibody
molecules
4
6 Second exposure
5
to the same antigen
First clone
Endoplasmic
reticulum
Plasma (effector) cells secreting antibodies
Second clone
Clone of plasma (effector) cells
secreting antibodies
Memory cells
Clone of memory cells
Figure 24.7A_s1
Primary immune response
1
B cells with
different
antigen
receptors
Antigen
receptor
on the cell
surface
Figure 24.7A_s2
Primary immune response
1
B cells with
different
antigen
receptors
Antigen
receptor
on the cell
surface
2
Antigen
molecules
Figure 24.7A_s3
Primary immune response
1
B cells with
different
antigen
receptors
Antigen
receptor
on the cell
surface
2
Antigen
molecules
3
Cell activation:
growth, division,
and differentiation
First exposure
to the antigen
Figure 24.7A_s4
Primary immune response
1
B cells with
different
antigen
receptors
Antigen
receptor
on the cell
surface
2
Antigen
molecules
3
First exposure
to the antigen
Cell activation:
growth, division,
and differentiation
Antibody
molecules
4
5
First clone
Endoplasmic
reticulum
Plasma (effector) cells secreting antibodies
Memory cells
Figure 24.7A_s5
Antigen
molecules
6
Memory cells
Second
exposure
to the same
antigen
Figure 24.7A_s6
Secondary immune response
Antibody
molecules
Antigen
molecules
6
Memory cells
Second
exposure
to the same
antigen
Clone of plasma (effector) cells
secreting antibodies
Second clone
Clone of memory cells
Figure 24.7B
Antibody concentration
Second exposure
to antigen X,
first exposure
to antigen Y
Secondary immune
response to
antigen X
First exposure
to antigen X
Primary immune
response to
antigen X
Antibodies
to Y
Antibodies
to X
0
7
14
21
Primary immune
response to
antigen Y
35
28
Time (days)
42
49
56
Figure 24.9
Binding of antibodies to antigens
inactivates antigens by
Neutralization
(blocks viral binding sites;
coats bacteria)
Virus
Agglutination
of microbes
Precipitation of
dissolved antigens
Activation of the
complement system
Complement
molecule
Bacteria
Antigen
molecules
Bacterium
Foreign cell
Enhances
Leads to
Phagocytosis
Cell lysis
Macrophage
Hole
Humoral vs. Cellular Response
Antibody reacts to Antigen in
blood, lymph & tissue fluids
Triggers B cells to clone itself
plasma cells make Antibody
that binds to pathogen
memory cells-perpetuate
clone & reduce response
time at 2nd exposure
T cell receptor recognizes
Antigen + MHC (me signal)
Triggers T cells to clone itself
T-cytotoxic –destroys cells
with MHC1 + antigen
T-helper-alerted by MHC2 +
antigen-stimulates B cells to
proliferate
T-suppressor-turn off
response
Figure 24.11
Phagocytic cell
(yellow) engulfing
a foreign cell
Self-nonself
complex
Macrophage
Microbe
B cell
T cell
receptor
Interleukin-2
stimulates
cell division
5
3
1
2
Helper
T cell
4
6
7
Interleukin-2
activates B cells
and other T cells
Self protein
Antigen from the microbe
(nonself molecule)
Antigen-presenting
cell
Interleukin-1
stimulates the
helper T cell Binding
Binding
site for the
self protein
site for the
antigen
Humoral
immune
response
(secretion of
antibodies by
plasma cells)
Cytotoxic
T cell
Cell-mediated
immune
response
(attack on
infected cells)
Figure 24.11_1
Self-nonself
complex
Macrophage
Microbe
3
1
2
Self protein
Antigen from the microbe
(nonself molecule)
Antigen-presenting
cell
Figure 24.11_2
Self-nonself
complex
B cell
T cell
receptor
Interleukin-2
stimulates
cell division
5
3
2
4
Antigenpresenting
cell
Helper
T cell
6
7
Interleukin-2
activates B cells
and other T cells
Binding
Cytotoxic
site for the
T cell
self protein
Interleukin-1
stimulates the
helper T cell Binding
site for the
antigen
Figure 24.12_s1
1 A cytotoxic T cell binds
to an infected cell.
Self-nonself
complex
Infected cell
Perforin
molecule
Foreign
antigen
Cytotoxic
T cell
Figure 24.12_s2
1 A cytotoxic T cell binds
to an infected cell.
Self-nonself
complex
Infected cell
Perforin
molecule
2
Perforin makes holes in the
infected cell’s membrane,
and an enzyme that
promotes apoptosis enters.
A hole
forming
Foreign
antigen
Cytotoxic
T cell
Enzymes that
promote
apoptosis
Figure 24.12_s3
1 A cytotoxic T cell binds
to an infected cell.
Self-nonself
complex
Infected cell
Perforin
molecule
2
Perforin makes holes in the
infected cell’s membrane,
and an enzyme that
promotes apoptosis enters.
A hole
forming
Foreign
antigen
Cytotoxic
T cell
Enzymes that
promote
apoptosis
3 The infected cell
is destroyed.
Problems
• Allergy-hypersensitive immune repsonse
– stimulates release of histamine b/c of antigenantibody interaction (immediate response)
– T cell response initiated (delayed response)
• Autoimmune
– fail to destroy antibody producing cell that matches to
self antigens
– virus antigen resembles self antigen
– T cells recognize antigen (non-self) that has a portion
similar to self antigen
Figure 24.17
Sensitization: Initial exposure to an allergen
Later exposure to the same allergen
B cell
(plasma cell)
Mast
cell
Antigenic determinant
1 An allergen (pollen
grain) enters the
bloodstream.
2 B cells make
antibodies.
Histamine
3 Antibodies
attach to a
mast cell.
4 The allergen binds
to antibodies on
a mast cell.
5 Histamine is
released, causing
allergy symptoms.