07. immunology
TRANSCRIPT
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Dr Alan Tuffery — Physiology Medical Science — 7 1
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Lecture 7 — ImmunologyStructure
• 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 lymphoidtissues and outline their roles
2. List the differences betweeninnate and adaptive immunity
3. Outline some key processesof innate immunity
4. Explain some key features ofadaptive immunity
5. Explain the pathophysiologyof some immune disorders.
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A network of cells and tissues that:1. Defends the body against invading pathogens2. Removes ‘worn-out’ cells3. Destroys abnormal/mutant cells within the
body (e.g. control of cancer)
Immune System can also have harmful effects:1. Allergies / autoimmune diseases2. Tissue rejection.
Role of the Immune System (IS)
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FUNGUSEpidermophyton
floccosum(athlete’s foot)
VIRUS
Polio
PARASITETapeworm
BACTERIAStaphylococcus
aureus(causes sepsis)
Infection-causing organisms (Pathogens)
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Components — White Blood Cells
Lymphocyte
– B cells - secreteantibodies
– T cells - directly destroyforeign cells
– Natural Killer cells - fightviruses
Monocyte/macrophage
– Phagocytosis– Secrete cytokines
(signalling moleculesother than antibodies).
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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
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Components — self-recognitionMajor Histocompatibilty Complex
• MHC on every (nucleated) cell
– Also known as humanleukocyte associated antigens(HLA)
• Normally the body’s immunesystem does not attack cellsthat carry this ‘self’ markeri.e. MHC
• No two individuals, exceptidentical twins, will evershare identical MHC.
Transplant rejection
– Organ transplants and skin graftsmay be rejected due to presence ofMHC
– To minimise rejection, the MHC ofdonor and recipient are matched asclosely as possible i.e. tissue typing
– Siblings usually provide the closestmatch
– MHC do not play a role in transfusionreactions because red blood cells donot have MHC.
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Skin & mucous membranesPhagocytosisInflammation
IMMUNE SYSTEM
INNATEINNATE IMMUNITY IMMUNITY(non-specific; natural)
ADAPTIVE IMMUNITY(specific; acquired)
HUMORAL-MEDIATED(antibody mediated)
B cells
CELL-MEDIATED
T cells
Organisation of the Immune System
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Innate vs Adaptive ImmunityInnate
(Phagocytosis, Inflammation)
• Nonspecific– Defends against any
pathogen upon firstexposure
– Responds to infectiousagents, chemical irritants,tissue injury, burns
Adaptive(Lymphocytes)
• Specific– Responds to specific
pathogens on 2nd orlater exposure
– Comes into play afternonspecific responseshave begun.
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• Initial & immediate response against invasion by avariety of pathogens
• The response is rapid and non-specific
• Main mechanisms1. Interferon, NK cells and complement system2. Phagocytosis (by neutrophils & macrophages)3. Inflammation.
Innate Immunity
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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 andcytotoxic T cells (qv)
Natural Killer cells
• Attack virus-infected cells…
• …Cause lysis
• NB Both IF and NKcells are non-specific— any virus.
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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!].
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Innate — 2. Phagocytosis
Stages of Phagocytosis1. Attachment2. Internalisation (0.1 s)3. Degradation4. Exocytosis.
SEM macrophage engulfing bacteria
S&G. 23.3
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Innate — 3. Inflammatory Response
1. Bacteria enter tissue/damage2. Release of histamine
– Increased blood flow– Increased vascular
permeability3. Increased leucocytes at site
Results– Destroy or inactivate invaders- Remove débris- Prepare for healing & repair.
Atopic_Dermatitis www.gcarlson.com
Animation of allergic (atopic) response
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Adaptive Immunity1. Specificity
• Lymphocytes (B and T cells) bind and respond to foreignmolecules 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 cellsreact more quickly & stronger response
• Self-Tolerance• Lymphocytes can distinguish ‘self’ (our normal antigens) from
‘non-self’ (antigens from foreign material).
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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&G
23.7 (see Sherw
ood 12-11)
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• T cells must becomeactivated before theycan attack pathogens
• The antigen is‘presented’ to the Tcell by an ANTIGENPRESENTING CELL(e.g. an infectedmacrophage) via itsMHC
Adaptive — Cell-mediated Immunity
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• 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, helperT cells and cytotoxic T cells; inhibit phagocytosis.
Activated T cell enlarges & divides into:
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Adaptive Immunity
Natural
ACTIVE PASSIVEAntibodies or
lymphocytes are produced as a
result of infection
Antibodies are passed to foetus
via placenta or colostrum
Artificial
ACTIVE PASSIVE
Antibodies areproduced as a
result of immunisation with a vaccine
Antibodies that have been produced
by another animal or given artificially.
Adaptive Immunity can beNATURALNATURAL or ARTIFICIALARTIFICIAL
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DISEASEDISEASE
• Systemic lupuserythematosus (SLE)
• Rheumatoid arthritis (RA)
• Multiple sclerosis (MS) (p116)
SYMPTOMSSYMPTOMS
• fever, arthritis, mouth ulcers,
• inflammation and damage tothe 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
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• 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 andother diseases develop.
Immune Disorders - AIDS
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SYMPTOMS
HIV Fatigue, fever, swollen glands, headache
AIDS Swollen lymph nodes, decreased T cell count;Susceptibility to pneumonia and Kaposi sarcoma;AIDS dementia
TRANSMISSIONThrough blood, semen, vaginal secretions and breast milk.
Immune Disorders - AIDS
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Learning Outcomes1. 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.