Lec 1- introduction to immunology Flashcards

1
Q

What is immunology

A
  • The study of defence against disease

- The study of the immune system

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2
Q

Defence against disease

A

What causes disease

  • Usually micro-organisms
  • For them, the human body is their ideal environment to grow
  • Adult gut- >500 microbial species (1kg in weight): these are commensal organisms so are friendly
  • We have evolved with these and we need them they protect against infection
    1) competition for space
    2) Production of antibacterials- colicin
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3
Q

Why are anti-biotics bad

A
  • They destroy our commensal and unbalanced the microflora of the gut
  • This then leaves us more exposed to infection by a more dangerous bacteria including C.difficle
  • Can lead to the deterioration of the epithelial linning meaning that the blood vessels are exposed so blood can enter into the gut and microbes can enter blood to be circulated
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4
Q

Disease causing microbes

A

1) bacteria
2) virus
3) Fungi
4) parasites

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5
Q

How are we protected

A

-We have multi-layered defence system to protect us from pathogens invasion
Mechanical defence: Epithelial cells
Chemical barrier: pH barriers, fatty acids, salivary
Microbial barrier

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6
Q

What happens if these barriers are breached

A

Innate immunity

  • Reacts quickly
  • Recognises a pathogen (non-specific)
  • Destroys the invaders
  • Induces the inflammatory response
  • Informs adaptive immunity
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7
Q

Pathogens are recognised and destroyed

A
  • Bacterial cell surface induces cleavage and activation of complement
  • One complement fragment covalently bonds to the bacterium, the other attracts an effector cell
  • The complement receptor on the effect cell binds to the complement fragment on the bacterium
  • Effector cell engulfs the bacterium , kills it and breaks it down
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8
Q

The inflammatory response

A
  • Healthy skin is not inflamed
  • Surface would introduced bacteria, which activate resident effector cells to secrete cytokines
  • Vasodilation and increased vascular permeability allow fluid, protein, and inflammatory cells to leave the blood and enter the tissue
  • Infacted tissue becomes inflamed, causing redness, heat, swelling and pain
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9
Q

Adaptive immunity

A
  • Innate Immunity can limit infection but it needs some help to eradicate infection- this is where adaptive immunity comes in
  • Adaptive immunity is:
  • provided by lymphocytes
  • Adapts to pathogens (highly specific)
  • Long-lasting memory cells
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10
Q

Effector mechanism in adaptive immunity

A
  • Progenitor cells give rise to lymphocytes with different specificity
  • Detection of a foreign anti-gun (pathogen) by the specific lymphocyte
  • Clonal selection
  • Activation results in proliferation and differentiation to many effector cells specific for the infection
  • Clonal expansion
  • Infection terminated
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11
Q

Clonal selection and expansion

A
  • A single progenitor cell gives rise to a large number of lymphocytes, each with a different specificity
  • Removal of potentially self reactive immature lymphocytes by clonal deletion (use of self antigens)
  • Pool of mature lymphocytes clonal selection (use of foreign antigen)
  • Proliferation and differentiation of activated specific lymphocytes to form a clone of effector cells
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12
Q

Adaptive immunity improves with age

A

-Primary immune response- first encounter with a pathogen
+Longer lag time
+Less specific response
-Secondary immune response- Second and subsequent infection with the same pathogen
+Faster response
+More specific response
+Principle of vaccination

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13
Q

2 immune systems are better than one

A
  • Look at BB slide
  • If we only have innate immunity , we will quickly deal with initial microbes we have no long lasting effects so microbes will overwhelm
  • If we have adaptive immunity only we are OK to start with, but because we don’t have the same amount of protection from innate the level of activation of adaptive immunity is reduced
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14
Q

All immune system cells derive from haematopoietic stem cells

A
  • Haematopoiesis is formation of blood cells- red and white
  • White blood cells- leukocytes- immune system cells
  • Haematopoiesis shifts during development- yolk sac, liver, spleen, bone marrow
  • Haematopoiesis occurs throughout life in bone marrow
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15
Q

All immune system cells derive from stem cell

A

1) Haematopoietic stem cell
2) Myeloid progenitor OR lymphoid progenitor
Lymphoid progenitor can produce
-NK cells
-T cell: helper or killer
-B cell
-Dendritic cells

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16
Q

Characteristics of leukocytes

A

1) Neutrophils 40-75% of cells; phagocytosis- rapid mobilisation
2) Lymphocyte 20-50%; adaptive immunity- specific cell surface receptors
3) Monocytes 2-10%; macrophage precursor- general scavengers
4) Eosinophil 1-6%; parasite defence
5) Basophil <1%; unknown

17
Q

Neutrophils fight and die

A
  • Large reserves of neutrophils are stored in the bone marrow and are released when needed to fight infection
  • Neutrophils treve to and enter the infected tissue
  • Where they engulf and kill bacteria
  • The neutrophils die in the tissue and are engulfed and degraded by macrophages
18
Q

Macrophages; fight and live

A
  • Binding of bacteria to phagocytic receptors on macrophages induces their engulfment and degradation
  • Binding of bacterial components to signalling receptors on macrophages induces synthesis of cytokine release which starts to recruit more cells
19
Q

Lymphocytes can be T or B

A

Several sub-lineages of lymphocytes

  • T cells: surface T cell receptor (TCR) and these will be either cytotoxic or helper
  • B Lymphocytes: these have surface immunoglobulins (BCR); differentiate to plasma cells
  • Plasma cells mass produce immunoglobulin as anti-bodies
20
Q

Lymphocytes

A

-Lymphocytes develop and mature in primary lymphoid tissue- bone marrow and thymus
B and T cells originate in bone marrow
-B cells remain there for their maturation
-T cells go to the thymus to be educated
-All other lymphoid tissues are secondary lymphoid tissues
-here, mature lymphocytes respond to pathogens

21
Q

Lymphatic circulation

A
  • Plasma leads from blood vessels- lymph or tissue fluid
  • Lymph is collected via lymph nodes, into lymphatic vessels
  • Lymph is returned to the blood through the thoracic duct
  • Flow of lymph is driven by movement rather than a pump (like the heart) and controlled by one-way valves
22
Q

Lymphatic recirculation

A
  • Lymphocytes move around the body in blood and lymph
  • Activated lymphocytes remain in the lymph nodes
  • Non-activated lymphocytes leave in lymph to be returned to the blood
  • So when a inactive lymphocyte is activated by a pathogen, it then travels to the lymph node where it educates other lymphocytes
23
Q

Lymph nodes- maximise cell encounter

A

-Different areas have different lymphocytes

24
Q

Adaptive immunity happens in 2ndary lymphoid tissue

A
  • Lymphocytes and lymph return to blood via the thoracic duct
  • Naive lymphocytes enter lymph nodes from the blood
  • Antigens from sites of infection reach lymph nodes via lymphatics
25
Q

Adaptive immunity happens in secondary lymphoid tissue

A
  • Pathogens are carried in lymph to the draining lymph nodes by immune cells (dendritic cells)
  • Dendritic cells meet with T cells and activate the pathogen specific ones
  • Effector T cells leave the lymph to go and fight in the tissues
  • Helper T cells activate pathogen-specific B cells in lymph nodes
  • B cells become plasma cells, make anti-bodies against infection
26
Q

Vulnerable surfaces are the most highly protected

A
  • Most secondary lymphoid tissue is associated with the mucosal surfaces (MALT)
  • Gut-associated lymphoid tissue (GALT)
  • Bronchial- associated lymphoid tissue (BALT)
27
Q

Defects in immunity

A

-Defects in immunity can be genetic (inherited) or induced (Disease)
Genetic-primary immunodeficiencies
-A wide range of severities depending on where the genetic lesion is
-Used to be fatal, now more promising treatments (from anti-biotics to bone marrow transplants)
Induced-secondary immunodeficiencies
-HIV causing aids
-HIV infects Th cells
-Increased susceptibility to disease