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Immune System
•Skin
pH=3-5
•Secretions
•Lysozyme
•Tears
•mucus,
•saliva
Mucus Membranes
Phagocytic cells
Migrate OUT of the blood when the sense differences
in concentration of certain chemicals engulf
bacteria, dead cells, etc….
Recognize surface
molecules on
abnormal cells
(cancerous or virus
infected)
Pin
Swelling
Skin surface
Bacteria
Chemical
signals
Phagocytes and
fluid move
into area
Phagocytes
White
blood cell
Blood vessel
1
Tissue injury; release of
chemical signals such as
histamine
link
2
Dilation and increased
leakiness of local blood
vessels; migration of
phagocytes to the area
3
Phagocytes
(macrophages and
neutrophils) consume
bacteria and cell
debris; tissue heals
Fig. 24-2a
Pin
Skin surface
Bacteria
Chemical
signals
White
blood cell
Blood vessel
1
Tissue injury; release of
chemical signals such as
histamine
Fig. 24-2b
Swelling
Phagocytes and
fluid move
into area
2
Dilation and increased
leakiness of local blood
vessels; migration of
phagocytes to the area
Fig. 24-2c
Phagocytes
3 Phagocytes (macrophages
and neutrophils) consume
bacteria and cell debris;
tissue heals
Lymphatic system
includes: -vessels (with valves)
-fluid (lymph)
-organs
Important cells involved are T lymphocytes and B lymphocytes
These cells are
responsible for
specific immune
responses to
specific
pathogens
Acquired Immunity (the immune
response)
•Is highly specific
•Produces antibodies in response to specific
antigens
•Antigens may be molecules on bacteria,
viruses, protozoa, worms, transplanted
organs
•Both B and T lymphocytes have receptors on
membrane that recognize different antigens
B cells
-mature in bone
- produce antibodies
-antibodies float through the blood,
recognizing and attaching to antigens
T cells
-mature in thymus
-do not produce antibodies
-cytotoxic T cells
- require cell/cell contact to destroy pathogen
Both B cells and T cells can produce memory cells
Fig. 24-5a
Cell-mediated
immune response
Humoral immune
response
Bone
marrow
Stem cell
Thymus
Via
blood
Immature
lymphocytes
Antigen
receptor
Antigen
receptor
B cell
T cell
Via
blood
Lymph nodes,
spleen, and
other lymphatic
organs
Final maturation
of B and T cells in
lymphatic organ
Fig. 24-5a
Cell-mediated
immune response
Humoral immune
response
Bone
marrow
Stem cell
Thymus
Via
blood
Immature
lymphocytes
Antigen
receptor
Antigen
receptor
B cell
T cell
Via
blood
Lymph nodes,
spleen, and
other lymphatic
organs
Final maturation
of B and T cells in
lymphatic organ
T cells are selected
B cells are selected
-antibody producing plasma
cells are produced
Person feels ill while these cells are produced
Symptoms diminish as these cells do their job
Response is much faster
Memory cells are activated
-tend to have a stronger response
than the primary
Fig. 24-7aa-1
Primary immune
response
B cells with
different
antigen
receptors
1
Antigen receptor
(antibody on cell
surface)
Fig. 24-7aa-2
Primary immune
response
B cells with
different
antigen
receptors
1
Antigen receptor
(antibody on cell
surface)
2
Antigen
molecules
Fig. 24-7aa-3
Primary immune
response
B cells with
different
antigen
receptors
1
Antigen receptor
(antibody on cell
surface)
2
Antigen
molecules
3 First exposure
to antigen
Cell activation:
growth,
division, and
differentiation
Fig. 24-7aa-4
Primary immune
response
1
B cells with
different
antigen
receptors
Antigen receptor
(antibody on cell
surface)
2
Antigen
molecules
3 First exposure
to antigen
Cell activation:
growth,
division, and
differentiation
Antibody
molecules
4
First clone
Endoplasmic
reticulum
Plasma (effector) cells secreting antibodies
Fig. 24-7aa-5
Primary immune
response
1
B cells with
different
antigen
receptors
Antigen receptor
(antibody on cell
surface)
2
Antigen
molecules
3 First exposure
to antigen
Cell activation:
growth,
division, and
differentiation
Antibody
molecules
4
First clone
5
Endoplasmic
reticulum
Plasma (effector) cells secreting antibodies
Memory cells
Fig. 24-7aa-6
Antigen
molecules
6 Second exposure
to same antigen
Secondary
immune
response (May
occur long after
primary immune
response.)
Antibody
molecules
Endoplasmic
reticulum
Second clone
Plasma (effector) cells secreting antibodies
Memory cells
Fig. 24-12-1
1
T cells work by directly binding to infected cells
and then destroying them
Cytotoxic T cell binds
to infected cell
Self-nonself
complex
Infected cell
Perforin
molecule
Foreign
antigen
Cytotoxic
T cell
Fig. 24-12-2
1
Cytotoxic T cell binds
to infected cell
Self-nonself
complex
Infected cell
Foreign
antigen
Perforin
molecule
Cytotoxic
T cell
2 Perforin makes holes in
infected cell’s membrane
and enzyme enters
Hole
forming
Fig. 24-12-3
1
Cytotoxic T cell binds
to infected cell
Self-nonself
complex
Infected cell
Foreign
antigen
Perforin
molecule
Cytotoxic
T cell
2 Perforin makes holes in
infected cell’s membrane
and enzyme enters
Hole
forming
3 Infected cell
is destroyed
Allergies
Hypersensitivity to environmental antigen
(allergen)
Antibodies attach to mast cells
- later, allergen attaches to these antibodies
on mast cells
Histamine & other inflammatory agents released
Fig. 24-17a
B cell
(plasma cell)
Mast
cell
Antigenic determinant
1
Histamine
3 Antibodies
attach to
mast cell
Sensitization: Initial exposure to allergen
Allergen (pollen grain) 2 B cells make
enters bloodstream
antibodies
Fig. 24-17b
4 Allergen binds to
5 Histamine is
released, causing
antibodies on
allergy symptoms
mast cell
Later exposure to same allergen
Anaphylactic shock
Acute reaction to allergen
Massive dilation of blood vessels
-drop in blood pressure
Counteracted by epinephrine
Active immunity
results from natural recovery from infections
vaccinations
Passive immunity
Receive antibodies from someone else
-IgG anitibodies cross placenta
-breast milk
-shots (rabies treatment)
Transfusions/transplants
ABO blood group
-IgM
doesn’t cross placenta
Antibodies produced against bacterial antigens
which are very similar
rH factor
-IgG  crosses placenta
Tissue graphs/ organ transplants
Give drugs that suppress cell mediated immunity
Bone marrow transplants
Risk of graft vs host reaction
Donor lymphocytes attack host cells
Autoimmune diseases
Immune system doesn’t recognize “self” and attacks
MS
Insulin dependent diabetes
HIV infection of cells require CD4
-found on T cells
Is a retrovirus
Antibodies are ineffective because
-provirus gives it “invisibility”
-rapid rate of mutation
-Helper T cells decrease
-secondary infections
Drug treatments slow viral replication
-AZT (reverse transcriptase inhibitors)
-protease inhibitors