Immunity Flashcards

1
Q

What are the two resistances to disease?

A

Non specific – innate defences

Specific resistance – adaptive – humoral and cellular

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2
Q

Whats the first line of defence in the innate non-specific defence?

A

First line of defence
- **Mechanical barriers **– skin (sebum - unsaturated fat that bacteria and pathogens don’t want to grow on also pH isn’t optimum either known as acid mantle (not conducive for growth) and mucous membranes (eg. respiratory tract)
- **Chemical barriers **– stomach acid (1.2-3pH also enzymes and mucus) and lysozyme (tears and saliva)

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3
Q

Whats the second line of defence in the innate non-specific defence?

A
  • Antimicrobial proteins – stomach interferon (antiviral), complement (enhances immune response) and transferring (inhibit certain bacterial growth)
  • **National killer cells **(NK cells) – destroys cells by perforating (perforin) the plasma membrane – making leaky – apoptosis
  • Phagocytes – engulf cells (can be fixed or wandering macrophages
  • Inflammation – redness, pain, heat and swelling
  • Fever – (slight increase actually beneficial as efficient immune system and pathogens more sluggish) thermostat in hypothalamus reset to higher level increases temperature enhances interferon inhibits some microbial growth and speeds up repair
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4
Q

Explain phagocytosis

A
  1. Phagocyte adheres to pathogen or debris
  2. Phagocyte forms pseudopods engulfed by particles forming phagosome
  3. Lysosome fuses with phagocytic vesicle forming phagosome
  4. Toxic compounds and lysosomal enzymes destroy pathogens
  5. Sometimes exocytosis of vesicle removes indigestible and residual material
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5
Q

What characterises adaptive defences?

A
  • Against specific invading agents such as bacteria, viruses, toxins or foreign tissues
  • Characterised by:
    1. Specificity – invading agent is recognised and dealt with
    2. Memory – second response is faster and greater than first (secondary immune response)
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6
Q

Whats an antigen?

A

Invading agents that are recognised as being non-self cells

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7
Q

What are lymphocytes?

A

Originate in bone marrow and carry out specific resistance

When matured the require specific antigen receptors to recognise specific invading agent
- immunocompetence (detect different pathogens)
- self-tolerance (recognise non-self cells)

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8
Q

What is immunocompetence?

A

detecting different pathogen

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9
Q

What is self-tolerance?

A

recognising non-self cells

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10
Q

What are two types of cells in the formation of lymphocytes?

A
  • B cells – B lymphocytes -remain in red blood cells
  • T cells – T lymphocytes – go to thymus
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11
Q

What are B cells?

A
  • Stimulates by antigen the B cells clone and become plasma cells
  • Produce antibodies known as immunoglobulins
  • This is known as antibody mediated or humoral response
  • Antibodies neutralise antigens
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12
Q

What are antigen actions that enhance phagocytosis?

A
  • Neutralisation (bind to active site and slows down masking dangerous bacterial exotoxins and viruses) – enhances phagocytosis
  • Agglutination – cell bound antigens (blood stick together) – enhances phagocytosis
  • Precipitation – soluble antigens – enhances phagocytosis
  • Fixes and activated complement leading to cell lysis and inflammation
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13
Q

Why are antibodies produced?

A
  • Specific antigen identified by specific B lymphocytes
  • B cells form clone and become plasma cells (and memory cells)– which secrete antibodies
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14
Q

What are the 5 classes of antibodies?

A
  • IgG – main antibody passing across placenta
  • IgA – secrete antibody
  • IgM – release into plasma, indicates current infection
  • IgE associated with allergies and parasitic infections
  • IgD – attached to B cells and acts as antigen receptor
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15
Q

What are T cells?

A
  • Have migrated to thymus – in cell mediated response
  • Directed against intracellular pathogens such as viruses, cancer cells and tissue transplants
  • Can become killer T cells – directly attack antigen
  • Or Helper T cells both antibodies mediated, and cell mediated responses
  • APC cell must tell T cell there’s a pathogen – present antigen to cell
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16
Q

What are major histocompatibility cells?

A

Protein attaching antigen and pathogen (makes clones and activates)
2 classes of MHC
1. Class 1 – activating T cells eventually becoming cytotoxic T cells
2. Class 2 – becoming helper T cells or regulatory T cells

17
Q

What are memory cells?

A
  • Secondary immune response
  • Both B and T cell reponsese produce memory cells – memory of invading antigen
  • Allows second or subsequent repsonse
  • So signs and symptoms of disease are not seen or are reduced
18
Q

State differences between active and passive humoural immunity

A

Active
- Naturally acquired – infection contact
- Articifically aquired – vaccine

Passive
- Naturally acquired – antibodies from mother to fetos
- Artifically acquired – infection of immune serum – gamma globulin

19
Q

What is the autoimmune response?

A
  • Body does not attack its own tissue as ‘self’ recognised
  • Immunological tolerance
  • When body fails to recognise self from non-self immune response attacks its own tissues
20
Q

What are examples of autoimmune response?

A
  1. **Multiple sclerosis **– destroy myelin of nervous system
  2. Rheumatoid arthritis – destroy cartikage in joints
  3. Type 1 diabetes mellitus – insulin producing cells in oancrease destroyed
  4. Glomerulonephritis – nephrons of kidney
  5. Myasthenia gravis – impaurs commynication between nerves and skeletal muscke by destroying receptor sites
21
Q

explain hypersensitivity as an immune response

A
  • Allergy occurs when person reacts to substance normally tolerated by most other people
  • Antigen = allergens
  • First and second exposure
  • First – sensitization stage – antigen invases, plasma cells made and attach – antibodies attach to other immune cells that are self cells
  • Subsequent exposure – memory cells have antibodies and anergen attach releasing overreaction of histome (too much)
22
Q

Examples of hypersensitivity

A
  1. Anaphylatic reactions – break mast cells
  2. Cytotoxic reactions – incompatible blood transfusion
  3. **Immune complex reactions **– destroy tissue eg. Rheumatoid arthritis and glomurelonephritis
  4. Delayed hypersensitivity reactions – 12-72 hours afterexposure eg. Mantoux skin test for TB
23
Q

What are cytotoxic T cells?

A

Kill target cells bearing specificic antigen while sparing neighboring uninfected cells – adaptive response

24
Q

What are helper T cells?

A

Sense theres infection in body – activate other immune cells to fight infection

25
Q

Whats specificity?

A

invading agent is recognised and dealt with

26
Q

Whats neutralisation?

A

(bind to active site and slows down masking dangerous bacterial exotoxins and viruses)
– enhances phagocytosis

27
Q

Explain mechanical barriers in non-specific immune response

A
  • skin (sebum - unsaturated fat that bacteria and pathogens don’t want to grow on also pH isn’t optimum either known as acid mantle (not conducive for growth)
  • mucous membranes (eg. respiratory tract)
28
Q

Explain chemical barriers in non-specific immune response

A
  • stomach acid (1.2-3pH also enzymes and mucus)
  • lysozyme (tears and saliva)
29
Q

What do national killer cells do in non-specific immune response?

A

– destroys cells by perforating (perforin) the plasma membrane
– making leaky
– apoptosis

30
Q

How does fever cause a non-specific immune response?

A
  • (slight increase in temperature actually beneficial as efficient immune system and pathogens more sluggish)
  • thermostat in hypothalamus reset to higher level increases temperature enhances interferon inhibits some microbial growth and speeds up repair