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Dr Alan Tuffery — Physiology Medical Science — 7 1
Slide 1
Lecture 7 — Immunology
Structure
• Components
– Leukocytes
– Lymphoid tissue
– Recognition of self
• Innate Immunity
– Physical and chemical barriers
– Phagocytosis
– Inflammation
• Adaptive immunity
– Humoral responses (B cells)
– Cell mediated responses (T
cells)
• Immune Disorders
– Autoimmune diseases
– AIDS
Learning Outcomes
1. List the principal lymphoid
tissues and outline their roles
2. List the differences between
innate and adaptive immunity
3. Outline some key processes
of innate immunity
4. Explain some key features of
adaptive immunity
5. Explain the pathophysiology
of some immune disorders.
Dr Alan Tuffery — Physiology Medical Science — 7 2
Slide 2
A network of cells and tissues that:
1. Defends the body against invading pathogens
2. Removes ‘worn-out’ cells
3. Destroys abnormal/mutant cells within the
body (e.g. control of cancer)
Immune System can also have harmful effects:
1. Allergies / autoimmune diseases
2. Tissue rejection.
Role of the Immune System (IS)
2
Dr Alan Tuffery — Physiology Medical Science — 7 3
Slide 3
FUNGUS
Epidermophyton
floccosum
(athlete’s foot)
VIRUS
Polio
PARASITE
Tapeworm
BACTERIA
Staphylococcus
aureus
(causes sepsis)
Infection-causing organisms (Pathogens)
Dr Alan Tuffery — Physiology Medical Science — 7 4
Slide 4
Components — White Blood Cells
Lymphocyte
– B cells - secrete
antibodies
– T cells - directly destroy
foreign cells
– Natural Killer cells - fight
viruses
Monocyte/macrophage
– Phagocytosis
– Secrete cytokines
(signalling molecules
other than antibodies).
3
Dr Alan Tuffery — Physiology Medical Science — 7 5
Slide 5
CENTRAL LYMPHATIC TISSUES
– Bone marrow - site of B cell development (and pre-
T cell)
– Thymus – site of T cell development
PERIPHERAL LYMPHATIC TISSUES
– Spleen
– Lymph nodes
– Gut-associated lymphatic tissue (GALT)
[Peyer’s Patches]
– Adenoids
– Appendix
– Tonsils.
Components — Lymphoid Tissues
Dr Alan Tuffery — Physiology Medical Science — 7 6
Slide 6
Components — self-recognition
Major Histocompatibilty Complex
• MHC on every (nucleated) cell
– Also known as human
leukocyte associated antigens
(HLA)
• Normally the body’s immune
system does not attack cells
that carry this ‘self’ marker
i.e. MHC
• No two individuals, except
identical twins, will ever
share identical MHC.
Transplant rejection
– Organ transplants and skin grafts
may be rejected due to presence of
MHC
– To minimise rejection, the MHC of
donor and recipient are matched as
closely as possible i.e. tissue typing
– Siblings usually provide the closest
match
– MHC do not play a role in transfusion
reactions because red blood cells do
not have MHC.
4
Dr Alan Tuffery — Physiology Medical Science — 7 7
Slide 7
Skin & mucous membranes
Phagocytosis
Inflammation
IMMUNE SYSTEM
INNATEINNATE IMMUNITYIMMUNITY
(non-specific; natural)
ADAPTIVE IMMUNITY
(specific; acquired)
HUMORAL-MEDIATED
(antibody mediated)
B cells
CELL-MEDIATED
T cells
Organisation of the Immune System
Dr Alan Tuffery — Physiology Medical Science — 7 8
Slide 8
Innate vs Adaptive Immunity
Innate
(Phagocytosis, Inflammation)
• Nonspecific
– Defends against any
pathogen upon first
exposure
– Responds to infectious
agents, chemical irritants,
tissue injury, burns
Adaptive
(Lymphocytes)
• Specific
– Responds to specific
pathogens on 2nd or
later exposure
– Comes into play after
nonspecific responses
have begun.
5
Dr Alan Tuffery — Physiology Medical Science — 7 9
Slide 9
• Initial & immediate response against invasion by a
variety of pathogens
• The response is rapid and non-specific
• Main mechanisms
1. Interferon, NK cells and complement system
2. Phagocytosis (by neutrophils & macrophages)
3. Inflammation.
Innate Immunity
Dr Alan Tuffery — Physiology Medical Science — 7 10
Slide 10
Innate — 1. Interferon, Natural Killer Cells
Interferon
• Released by virus-
attacked cells
• Protects other cells
from any virus
• Anti-cancer effects
– Slows cell division
– Enhances action of
NK cells and
cytotoxic T cells (qv)
Natural Killer cells
• Attack virus-
infected cells…
• …Cause lysis
• NB Both IF and NK
cells are non-specific
— any virus.
6
Dr Alan Tuffery — Physiology Medical Science — 7 11
Slide 11
Innate — 1. Complement System
Many very complex actions
• Innate response is recognition of micro-
organisms
• Lysis of invading micro-organisms
• Also reinforces other inflammatory
responses [hence name!].
Dr Alan Tuffery — Physiology Medical Science — 7 12
Slide 12
Innate — 2. Phagocytosis
Stages of Phagocytosis
1. Attachment
2. Internalisation (0.1 s)
3. Degradation
4. Exocytosis.
SEM macrophage engulfing bacteria
S&G. 23.3
7
Dr Alan Tuffery — Physiology Medical Science — 7 13
Slide 13
Innate — 3. Inflammatory Response
1. Bacteria enter tissue/damage
2. Release of histamine
– Increased blood flow
– Increased vascular
permeability
3. Increased leucocytes at site
Results
– Destroy or inactivate invaders
- Remove débris
- Prepare for healing & repair.
Atopic_Dermatitiswww.gcarlson.com
Animation of allergic (atopic) response
Dr Alan Tuffery — Physiology Medical Science — 7 14
Slide 14
Adaptive Immunity
1. Specificity
• Lymphocytes (B and T cells) bind and respond to foreign
molecules known as antigens via antigen receptors
1. 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
• Self-Tolerance
• Lymphocytes can distinguish ‘self’ (our normal antigens) from
‘non-self’ (antigens from foreign material).
8
Dr Alan Tuffery — Physiology Medical Science — 7 15
Slide 15
Adaptive Immunity— humoral (antibody-mediated)
1. B Cells — Clonal Selection
• Antigen fits B cell’s receptors
• Proliferation and differentiation
into …
1. Plasma cells
• Produce antibodies in blood
• (immunoglobulins IgG, IgM, IgE, IgA, IgD)
• Short-lived
2. Memory cells (clone)
• With same receptor
• Long-lived.
S&G23.7(seeSherwood12-11)
Dr Alan Tuffery — Physiology Medical Science — 7 16
Slide 16
• 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
Adaptive — Cell-mediated Immunity
9
Dr Alan Tuffery — Physiology Medical Science — 7 17
Slide 17
• CYTOTOXIC T CELLS
– kill infected cells by lysis (direct action)
• HELPER T CELLS (~70% of T cells)
– secrete cytokines that enhance the 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.
Activated T cell enlarges & divides into:
Dr Alan Tuffery — Physiology Medical Science — 7 18
Slide 18
Adaptive Immunity
Natural
ACTIVE PASSIVE
Antibodies or
lymphocytes are
produced as a
result of infection
Antibodies are
passed to foetus
via placenta
or colostrum
Artificial
ACTIVE PASSIVE
Antibodies are
produced as a
result of
immunisation
with a vaccine
Antibodies that
have been produced
by another animal
or given artificially.
Adaptive Immunity can be
NATURALNATURAL or ARTIFICIALARTIFICIAL
10
Dr Alan Tuffery — Physiology Medical Science — 7 19
Slide 19
DISEASEDISEASE
• Systemic lupus
erythematosus (SLE)
• Rheumatoid arthritis (RA)
• Multiple sclerosis (MS) (p116)
SYMPTOMSSYMPTOMS
• fever, arthritis, mouth ulcers,
• inflammation and damage to
the cartilage and bone of joints
• T cells attack myelin:
Blurred vision,
Muscle weakness,
Ataxia
If immune system does not recognise its ‘self’ (e.g.
MHC), it reacts against normal cells and tissues
Immune Disorders – Autoimmune Diseases
Dr Alan Tuffery — Physiology Medical Science — 7 20
Slide 20
• AIDS is caused by Human Immunodeficiency Virus (HIV)
• 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 T cell function is impaired, immune responses weaken and
other diseases develop.
Immune Disorders - AIDS
11
Dr Alan Tuffery — Physiology Medical Science — 7 21
Slide 21
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.
Immune Disorders - AIDS
Dr Alan Tuffery — Physiology Medical Science — 7 22
Slide 22
Learning Outcomes
1. List the principal lymphoid tissues and outline their roles
• Thymus (T cell dev.); Gut —B cells)
2. List the differences between innate and adaptive immunity
• Specificity, 1st exposure, cell-mediated, speed
3. Outline some key processes of innate immunity
• phagocytosis, inflammation, immune memory, self recognition)
4. Explain some key features of adaptive immunity
5. Explain the pathophysiology of some immune disorders.

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07. immunology

  • 1. 1 Dr Alan Tuffery — Physiology Medical Science — 7 1 Slide 1 Lecture 7 — Immunology Structure • Components – Leukocytes – Lymphoid tissue – Recognition of self • Innate Immunity – Physical and chemical barriers – Phagocytosis – Inflammation • Adaptive immunity – Humoral responses (B cells) – Cell mediated responses (T cells) • Immune Disorders – Autoimmune diseases – AIDS Learning Outcomes 1. List the principal lymphoid tissues and outline their roles 2. List the differences between innate and adaptive immunity 3. Outline some key processes of innate immunity 4. Explain some key features of adaptive immunity 5. Explain the pathophysiology of some immune disorders. Dr Alan Tuffery — Physiology Medical Science — 7 2 Slide 2 A network of cells and tissues that: 1. Defends the body against invading pathogens 2. Removes ‘worn-out’ cells 3. Destroys abnormal/mutant cells within the body (e.g. control of cancer) Immune System can also have harmful effects: 1. Allergies / autoimmune diseases 2. Tissue rejection. Role of the Immune System (IS)
  • 2. 2 Dr Alan Tuffery — Physiology Medical Science — 7 3 Slide 3 FUNGUS Epidermophyton floccosum (athlete’s foot) VIRUS Polio PARASITE Tapeworm BACTERIA Staphylococcus aureus (causes sepsis) Infection-causing organisms (Pathogens) Dr Alan Tuffery — Physiology Medical Science — 7 4 Slide 4 Components — White Blood Cells Lymphocyte – B cells - secrete antibodies – T cells - directly destroy foreign cells – Natural Killer cells - fight viruses Monocyte/macrophage – Phagocytosis – Secrete cytokines (signalling molecules other than antibodies).
  • 3. 3 Dr Alan Tuffery — Physiology Medical Science — 7 5 Slide 5 CENTRAL LYMPHATIC TISSUES – Bone marrow - site of B cell development (and pre- T cell) – Thymus – site of T cell development PERIPHERAL LYMPHATIC TISSUES – Spleen – Lymph nodes – Gut-associated lymphatic tissue (GALT) [Peyer’s Patches] – Adenoids – Appendix – Tonsils. Components — Lymphoid Tissues Dr Alan Tuffery — Physiology Medical Science — 7 6 Slide 6 Components — self-recognition Major Histocompatibilty Complex • MHC on every (nucleated) cell – Also known as human leukocyte associated antigens (HLA) • Normally the body’s immune system does not attack cells that carry this ‘self’ marker i.e. MHC • No two individuals, except identical twins, will ever share identical MHC. Transplant rejection – Organ transplants and skin grafts may be rejected due to presence of MHC – To minimise rejection, the MHC of donor and recipient are matched as closely as possible i.e. tissue typing – Siblings usually provide the closest match – MHC do not play a role in transfusion reactions because red blood cells do not have MHC.
  • 4. 4 Dr Alan Tuffery — Physiology Medical Science — 7 7 Slide 7 Skin & mucous membranes Phagocytosis Inflammation IMMUNE SYSTEM INNATEINNATE IMMUNITYIMMUNITY (non-specific; natural) ADAPTIVE IMMUNITY (specific; acquired) HUMORAL-MEDIATED (antibody mediated) B cells CELL-MEDIATED T cells Organisation of the Immune System Dr Alan Tuffery — Physiology Medical Science — 7 8 Slide 8 Innate vs Adaptive Immunity Innate (Phagocytosis, Inflammation) • Nonspecific – Defends against any pathogen upon first exposure – Responds to infectious agents, chemical irritants, tissue injury, burns Adaptive (Lymphocytes) • Specific – Responds to specific pathogens on 2nd or later exposure – Comes into play after nonspecific responses have begun.
  • 5. 5 Dr Alan Tuffery — Physiology Medical Science — 7 9 Slide 9 • Initial & immediate response against invasion by a variety of pathogens • The response is rapid and non-specific • Main mechanisms 1. Interferon, NK cells and complement system 2. Phagocytosis (by neutrophils & macrophages) 3. Inflammation. Innate Immunity Dr Alan Tuffery — Physiology Medical Science — 7 10 Slide 10 Innate — 1. Interferon, Natural Killer Cells Interferon • Released by virus- attacked cells • Protects other cells from any virus • Anti-cancer effects – Slows cell division – Enhances action of NK cells and cytotoxic T cells (qv) Natural Killer cells • Attack virus- infected cells… • …Cause lysis • NB Both IF and NK cells are non-specific — any virus.
  • 6. 6 Dr Alan Tuffery — Physiology Medical Science — 7 11 Slide 11 Innate — 1. Complement System Many very complex actions • Innate response is recognition of micro- organisms • Lysis of invading micro-organisms • Also reinforces other inflammatory responses [hence name!]. Dr Alan Tuffery — Physiology Medical Science — 7 12 Slide 12 Innate — 2. Phagocytosis Stages of Phagocytosis 1. Attachment 2. Internalisation (0.1 s) 3. Degradation 4. Exocytosis. SEM macrophage engulfing bacteria S&G. 23.3
  • 7. 7 Dr Alan Tuffery — Physiology Medical Science — 7 13 Slide 13 Innate — 3. Inflammatory Response 1. Bacteria enter tissue/damage 2. Release of histamine – Increased blood flow – Increased vascular permeability 3. Increased leucocytes at site Results – Destroy or inactivate invaders - Remove débris - Prepare for healing & repair. Atopic_Dermatitiswww.gcarlson.com Animation of allergic (atopic) response Dr Alan Tuffery — Physiology Medical Science — 7 14 Slide 14 Adaptive Immunity 1. Specificity • Lymphocytes (B and T cells) bind and respond to foreign molecules known as antigens via antigen receptors 1. 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 • Self-Tolerance • Lymphocytes can distinguish ‘self’ (our normal antigens) from ‘non-self’ (antigens from foreign material).
  • 8. 8 Dr Alan Tuffery — Physiology Medical Science — 7 15 Slide 15 Adaptive Immunity— humoral (antibody-mediated) 1. B Cells — Clonal Selection • Antigen fits B cell’s receptors • Proliferation and differentiation into … 1. Plasma cells • Produce antibodies in blood • (immunoglobulins IgG, IgM, IgE, IgA, IgD) • Short-lived 2. Memory cells (clone) • With same receptor • Long-lived. S&G23.7(seeSherwood12-11) Dr Alan Tuffery — Physiology Medical Science — 7 16 Slide 16 • 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 Adaptive — Cell-mediated Immunity
  • 9. 9 Dr Alan Tuffery — Physiology Medical Science — 7 17 Slide 17 • CYTOTOXIC T CELLS – kill infected cells by lysis (direct action) • HELPER T CELLS (~70% of T cells) – secrete cytokines that enhance the 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. Activated T cell enlarges & divides into: Dr Alan Tuffery — Physiology Medical Science — 7 18 Slide 18 Adaptive Immunity Natural ACTIVE PASSIVE Antibodies or lymphocytes are produced as a result of infection Antibodies are passed to foetus via placenta or colostrum Artificial ACTIVE PASSIVE Antibodies are produced as a result of immunisation with a vaccine Antibodies that have been produced by another animal or given artificially. Adaptive Immunity can be NATURALNATURAL or ARTIFICIALARTIFICIAL
  • 10. 10 Dr Alan Tuffery — Physiology Medical Science — 7 19 Slide 19 DISEASEDISEASE • Systemic lupus erythematosus (SLE) • Rheumatoid arthritis (RA) • Multiple sclerosis (MS) (p116) SYMPTOMSSYMPTOMS • fever, arthritis, mouth ulcers, • inflammation and damage to the cartilage and bone of joints • T cells attack myelin: Blurred vision, Muscle weakness, Ataxia If immune system does not recognise its ‘self’ (e.g. MHC), it reacts against normal cells and tissues Immune Disorders – Autoimmune Diseases Dr Alan Tuffery — Physiology Medical Science — 7 20 Slide 20 • AIDS is caused by Human Immunodeficiency Virus (HIV) • 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 T cell function is impaired, immune responses weaken and other diseases develop. Immune Disorders - AIDS
  • 11. 11 Dr Alan Tuffery — Physiology Medical Science — 7 21 Slide 21 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. Immune Disorders - AIDS Dr Alan Tuffery — Physiology Medical Science — 7 22 Slide 22 Learning Outcomes 1. List the principal lymphoid tissues and outline their roles • Thymus (T cell dev.); Gut —B cells) 2. List the differences between innate and adaptive immunity • Specificity, 1st exposure, cell-mediated, speed 3. Outline some key processes of innate immunity • phagocytosis, inflammation, immune memory, self recognition) 4. Explain some key features of adaptive immunity 5. Explain the pathophysiology of some immune disorders.