Download Guide 22

Bio 100 – Guide 22
Antigens have specific regions where antibodies
bind to them
• Antigens are usually molecules on the surface
of viruses or foreign cells
• Antigenic determinants are the specific
regions on an antigen to which antibodies bind
–Antigens may have several different
determinants
–Immune system may direct several distinct
antibodies against one antigen
Lymphocytes mount a dual defense
• Lymphocytes originate from stem cells
in the bone marrow
• Humoral immunity
–B cells secrete antibodies that circulate
in blood and lymph to sites of infection
–Defends primarily against bacteria and
viruses present in body fluids
LE 24-5a
Bone marrow
Thymus
Stem cell
Via
blood
Immature lymphocyte
Antigen
receptors
T cell
B cell
Humoral
immunity
Cell-mediated
immunity
Via
blood
Lymph nodes, spleen, and
other lymphatic organs
Other parts of the
lymphatic system
Final maturation
of B and T cells in
lymphatic organ
LE 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
Primary immune
response to
antigen Y
Antibodies
to Y
Antibodies
to X
0
7
14
21
28
35
Time (days)
42
49
56
BIG Questions
• What is the process by which
antibodies are made?
• What is the basis of Antigenic
Memory? This is very important
because it is the basis of
vaccination, one of our only
medical defenses against viruses.
Clonal selection musters defensive forces
against specific antigens
• Primary immune response: lymphocytes
exposed to antigen for the first time
–Antigen activates a small subset of
lymphocytes (B cells) bearing
complementary receptors
–The selected B cells multiply into
clones of effector and memory cells
• Secondary immune response
–Memory cells exposed to same antigen
a second time
–Second round of clonal selection
ensues
–Secondary response is faster and
stronger; produces very high levels of
antibodies
http://www.geneseo.edu/~simon/bio100/media/RoleOFBCells.html
LE 24-7a
Primary
immune
response
Antigen receptor
(antibody on cell
surface)
Antigen
molecules
First exposure
to antigen
Antibody
molecules
Endoplasmic
reticulum
Plasma (effector) cells secreting antibodies
Memory cells
Antigen
molecules
Second exposure
to same antigen
Secondary
immune
response
Antibody
molecules
Endoplasmic
reticulum
Plasma (effector) cells secreting antibodies
Memory cells
• Effector (plasma) cells
–Combat the antigen
–Secrete antibody molecules that
circulate in blood and contribute to
humoral immunity
–Last only 4 or 5 days
• Memory cells
–Remain in lymph nodes
–May last for decades, sometimes
confer lifetime immunity
Antibodies are the weapons of humoral immunity
• Antibody molecules are secreted by plasma
(effector) B cells
• Antibody molecule structure
–Y shaped, made of two identical "heavy"
and two identical "light" polypeptide chains
–a C (constant) and a V (variable) region on
each chain
–Antigen-binding sites specific to the
antigenic determinants that elicited its
secretion
LE 24-8b
Antigen-binding
sites
Light
chain
C
C
Heavy
chain
• Antibody functions in humoral
immunity
–Binds its antigen at the antigenbinding site
–Assists in elimination of the
antigen, at the C region of the
heavy chains
LE 24-6
Antibody A
molecules
Antigenbinding
sites
Antigenic
determinants
Antigen
molecule
Antibody B
molecule
Antibodies mark antigens for elimination
• Effector mechanisms involve a specific
recognition-and-attack phase followed by a
nonspecific destruction phase
• Antibodies mark invaders by forming
antigen-antibody complexes
• Binding triggers mechanisms to eliminate
the invader
–Neutralization
–Agglutination of microbes
–Precipitation of dissolved antigens
–Activation of complement system
http://www.geneseo.edu/~simon/bio100/media/24_09Antibodies_A.swf
LE 24-9
Binding of antibodies to antigens
inactivates antigens by
Neutralization
(blocks viral binding
sites; coats bacteria)
Agglutination
of microbes
Precipitation of
dissolved antigens
Complement
molecule
Bacteria
Virus
Antigen
molecules
Bacterium
Activation of
complement system
Foreign cell
Enhances
Leads to
Phagocytosis
Cell lysis
Macrophage
Hole
BIG Questions
• How Does the body distinguish
between self and non-self?
• Why don't we make antibodies
against our the molecules
(antigens) in our bodies?
The immune system depends on our molecular
fingerprints
• Each person's cells have particular self protein
"fingerprints" that mark them as off limits to
attack by lymphocytes
• Self proteins are coded for by MHC (major
histocompatibility complex) genes
–Except for identical twins, two individuals
cannot have identical self proteins
• Transplanted organs may be rejected because
their cells lack the unique fingerprint of the
recipient's self proteins
BIG Questions
• 1 B cell makes 1 Antibody.
• How is the body to be able to make
millions of different antibodies, even to
molecules never conceived?
• Where is the genetic information for
the differing variable ends on the
antibody molecule?
• Functioning of B and T cells
–Certain genes in the cell are turned on
–Cell synthesizes specific protein molecules,
which are incorporated into the plasma
membrane
–Antigen receptors sticking up from cell
surface recognize specific antigens and
mount a defense
• Millions of diverse B and T cells stand ready
to recognize and bind virtually every possible
antigen
• Cell-mediated immunity
–In the thymus, immature
lymphocytes specialize into T cells
–T cells attack cells infected with
pathogens, fungi and protozoans,
cancer cells
–T cells also promote phagocytosis
and production of antibodies
http://nobelprize.org/educational_games/medicine/immunity/images/detail/series.gif
Helper T cells stimulate humoral and cellmediated immunity
• Cell-mediated immunity produced by T cells
battles pathogens that have entered body cells
• T cells respond only to antigens present on the
surface of the body's own cells
–Cytotoxic T cells attack infected cells
–Helper T cells
• Help activate T cells, B cells, and
macrophages
• Interact with antigen-presenting cells
• Precise interaction of antigen-presenting cells
and helper T cells
–Antigen-presenting cell self protein binds
antigen nonself molecules and displays
them on the cell surface
–Helper T cells recognize and bind to the
self-nonself complex
• Depends on highly specific receptors in
the T cell's plasma membrane
–Binding activates helper T cells
• Enhanced by other signals
Helper T cells are the major driving force and
the main regulators of the immune defense.
Their primary task is to activate B cells and
killer T cells.
http://nobelprize.org/educational_games/medicine/immunity/images/detail/series.gif
LE 24-11
Self-nonself
complex
Microbe
Macrophage
B cell
T cell
receptor
Interleukin-2
stimulates
cell division
Helper
T cell
Humoral
immunity
(secretion of
antibodies by
plasma cells)
Interleukin-2
activates
other B cells
and T cells
Self protein
Antigen from microbe
(nonself molecule)
Antigen-presenting
cell
Interleukin-1
stimulates
helper T cell
Binding Binding
site for site for
antigen self protein
Cytotoxic
T cell
Cell-mediated
immunity
(attack on
infected cells)
Cytotoxic T cells destroy infected body cells
• Like helper T cells, cytotoxic T cells
recognize and bind with self-nonself
complexes on infected cells
• Mechanism of cytotoxic T cell action
–Binding to infected cell stimulates cytotoxic
T cell to synthesize perforin
–Perforin makes holes in infected cell's
membrane, and T cell enzymes enter
–Infected cell is destroyed
LE 24-13
Cytotoxic T cell binds
to infected cell
Perforin makes holes in
infected cell’s membrane
and enzyme enters
Self-nonself
complex
Infected cell
Perforin
molecule
Hole
forming
Foreign
antigen
Cytotoxic
T cell
Enzyme that
can promote
apoptosis
Infected cell
is destroyed
Cytotoxic T cells may help prevent cancer
• Genetic changes leading to cancer can
result in new proteins displayed on cell
surfaces
• T cells identify these tumor antigens as
foreign and destroy the affected cells
http://www.topnews.in/health/files/Allergy.jpg
Allergies are overreactions to certain
environmental antigens
• Allergies are abnormal sensitivities to
antigens (allergens) in the surroundings
• Allergic reactions occur in two stages
–Sensitization: initial exposure to allergen
• Allergen enters bloodstream
• B cells make antibodies
• Antibodies attach to mast cells that
produce histamines and trigger the
inflammatory response
–Later exposure to same allergen
• Allergen binds to antibodies on mast
cell
• Histamine is released, causing
allergy symptoms
• Anaphylactic shock is a severe allergic
reaction
–Causes severe drop in blood pressure
–Potentially fatal
LE 24-17
B cell
(plasma cell)
Mast
cell
Antigenic
determinant
Allergen (pollen
grain) enters blood
stream
B cells make
antibodies
Histamine
Antibodies
attach to
mast cell
Sensitization: Initial exposure to allergen
Allergen binds
to antibodies
on mast cell
Histamine is
released, causing
allergy symptoms
Later exposure to same allergen
The End