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Transcript
JS/DipEx
11/16/07
Slide 1
Lecture 11 —
Immunology 2
Adaptive immunity
Learning Outcomes
To b e ab le to:
• Humoral responses (B cells)
• Cell-mediated responses (T cells)
– Specificity
– Diversity
– Memory
– Self-Tolerance
1.
outline the principal properties
of Adaptive Immunity
2.
compare and contrast innate
and adaptive immunity
3.
explain the principal changes
in an immune disorder
4.
outline the functions of B cells
(incl. immune memory)
5.
outline functions of T cells.
– Humoral responses (B cells
• Immune Disorders
– Autoimmune diseases
– AIDS
Dr Alan Tuffery
JS/Dip Ex Tissue Structure — 11
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Slide 2
Innate vs Adaptive Immunity
(reprise)
Adaptive
Innate
(Lymphocytes)
(Phagocytosis, Inflammation)
• Nonspecific
• Specific
– Defends against any
pathogen upon first exposure
– Responds to:
– Responds to specific
pathogens on 2nd or
later exposure
• infectious agents
• chemical irritants
• tissue injury
• burns
Dr Alan Tuffery
– Comes into play after
nonspecific responses
have begun.
JS/Dip Ex Tissue Structure — 11
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JS/DipEx
11/16/07
Slide 3
Features of Adaptive Immunity
 Specificity
 Lymphocytes (B and T cells) bind and respond to foreign molecules
(antigens) via antigen receptors: each to a specific antigen
 Diversity
 The body possesses millions of lymphocytes that can recognise and
respond to millions of antigens (one each)
 Memory
 1st exposure to an antigen generates lymphocytes & long-lived
memory cells – next exposure to the same antigen, memory cells
react more quickly & stronger response (‘acquired immunity’)
 Self-Tolerance
 Lymphocytes can distinguish ‘self’ (our normal antigens) from ‘nonself’ (antigens from foreign material).
Dr Alan Tuffery
JS/Dip Ex Tissue Structure — 11
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Adaptive Immunity can be
NATURAL or ARTIFICIAL
Slide 4
Adaptive Immunity
Natural
Artificial
ACTIVE
ACTIVE
PASSIVE
Antibodies are
Antibodies or
lymphocytes are passed to foetus
via placenta
produced as a
or colostrum
result of infection
Dr Alan Tuffery
PASSIVE
Antibodies are
Antibodies that
produced as a have been produced
result of
by another animal
immunisation
or given artificially.
with a vaccine
JS/Dip Ex Tissue Structure — 11
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11/16/07
Slide 5
B Cells — Clonal Selection
• Antigen fits B cell’s receptors
• Proliferation and differentiation
into …
1. Plasma cells
• Produce antibodies in blood
• (immunoglobulins I gG, IgM, IgE, IgA, I gD)
• Short-lived
2. Memory cells (clone)
S&G 23.7 (G&S 23.8)
Dr Alan Tuffery
• With same receptor
• Long-lived.
JS/Dip Ex Tissue Structure — 11
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Slide 6
Immune Disorders – Autoimmune Diseases
If immune system does not recognise its ‘self’ (e.g. MHC),
it reacts against normal cells and tissues
DISEASE
SYMPTOMS
• Systemic lupus
erythematosus (SLE)
• fever, arthritis, mouth ulcers, etc
• Rheumatoid arthritis (RA)
• inflammation and damage to the
cartilage and bone of joints
• Multiple sclerosis (MS)
• T cells attack myelin:
– (G&S p689)
Dr Alan Tuffery
Blurred vision, muscle weakness, ataxia.
JS/Dip Ex Tissue Structure — 11
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JS/DipEx
11/16/07
Slide 7
Adaptive — Cell-mediated Immunity
 T cells must
S&G 23.10 (G&S 23.11)
become activated
before they can
attack pathogens
1. Cytotoxic T cells
 The antigen is
‘presented’ by an
infected cell via the
via its Class I MHC.
Dr Alan Tuffery
JS/Dip Ex Tissue Structure — 11
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Slide 8
Adaptive — Cell-mediated Immunity
2. Helper T Cell
S&G 23.10 (G&S 23.11)
– binds to Class II MHC
on an ANTIGEN
PRESENTING CELL
(e.g. an infected macrophage).
Dr Alan Tuffery
JS/Dip Ex Tissue Structure — 11
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11/16/07
Slide 9
Activated T Cell Responses
CYTOTOXIC T CELLS
 kill infected cells by lysis (direct
action) [pic] or apoptosis
HELPER T CELLS (~70% of T cells)
 secrete cytokines that enhance the
www.gcarlson.com

activity of cytotoxic T cells;
enhance phagocytosis
stimulate development of B cells
into plasma cells (indirect action)
SUPPRESSOR T CELLS
 secrete cytokines that:
 suppress the activity of B cells,
helper, T cells and cytotoxic T cells
 inhibit phagocytosis.
Dr Alan Tuffery
JS/Dip Ex Tissue Structure — 11
9
Slide 10
Immune Disorders — Autoimmune Diseases
If immune system does not recognise its ‘self’ (e.g. MHC),
it reacts against normal cells and tissues
DISEASE
SYMPTOMS
• Systemic lupus
erythematosus (SLE)
• fever, arthritis, mouth ulcers,
• Rheumatoid arthritis (RA)
• inflammation and damage to the
cartilage and bone of joints
• Multiple sclerosis (MS) (p116)
• T cells attack myelin:
Blurred vision,
Muscle weakness,
Ataxia
Dr Alan Tuffery
JS/Dip Ex Tissue Structure — 11
10
5
JS/DipEx
11/16/07
Slide 11
Immune Disorders - AIDS
 Human Immunodeficiency Virus (HIV) binds to the surface of helper
T cells and its nucleic acids (RNA and DNA) enter the T cell
 Inside the cell, HIV uses the cell to make copies of itself
 HIV slowly destroys Helper T cells in the body
 (Helper T cells = 70% of all T cells)
 When Helper T cell function is impaired, immune responses weaken
and other diseases develop.
Dr Alan Tuffery
JS/Dip Ex Tissue Structure — 11
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Slide 12
Immune Disorders - AIDS
SYMPTOMS
HIV
Fatigue, fever, swollen glands, headache
AIDS
Swollen lymph nodes, decreased T cell count;
Susceptibility to pneumonia and Kaposi sarcoma;
AIDS dementia
TRANSMISSION
Through blood, semen, vaginal secretions and breast milk
Further info (and animations):
www.biology.arizona.edu/immunology/tutorials/AIDS/response.html.
Dr Alan Tuffery
JS/Dip Ex Tissue Structure — 11
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JS/DipEx
11/16/07
Slide 13
Systemic Lupus Erythematosus (SLE)
Common Symptoms
• Painful or swollen joints and
muscle pain
• Unexplained fever
• Red rashes, mostly in the face
• Chest pain upon deep
breathing
• Unusual loss of hair
• Pale or purple fingers or toes
from cold or stress (Raynaud's
phenomenon)
Dr Alan Tuffery
•
•
•
•
•
•
•
•
Sensitivity to the sun
Swelling (edema) in legs or
around eyes
Mouth ulcers
Swollen glands
Extreme fatigue
Anaemia
Renal failure
Symptoms of lupus can range
from mild to severe and may
come and go over time.
JS/Dip Ex Tissue Structure — 11
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Slide 14
Learning Outcomes 1
To be able to:
1. outline the principal properties of Adaptive Immunity
Specificity, Diversity, Memory, Self-tolerance
2. compare and contrast innate and adaptive immunity
Specific — non-specific; 1st — 2nd exposure; fast — slow
3. explain the principal changes in an immune disorder
E.g. HIV kills helper T cells — reduced immune competence.
Dr Alan Tuffery
JS/Dip Ex Tissue Structure — 11
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JS/DipEx
11/16/07
Slide 15
Learning Outcomes 2
To be able to:
4. outline the functions of B cells (incl. immune memory)
Produce antibodies (plasma cells); form memory cells
5. outline functions of T cells
Cytotoxic T: lyses infected cells
Helper T: enhance cytotoxic T, phagocytosis; stim B cells
(Ab)
Suppressor T: suppress all above.
Dr Alan Tuffery
JS/Dip Ex Tissue Structure — 11
15
Slide 16
Cell-Mediated Immunity
•
T cells must become
activated before they
can attack pathogens
•
The antigen is
‘presented’ to the T cell
by an ANTIGEN
PRESENTING CELL
(e.g. an infected
macrophage) via its
MHC.
Dr Alan Tuffery
www.gcarlsoncom
JS/Dip Ex Tissue Structure — 11
16
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