Innate immunity Flashcards

1
Q

What are the 3 phases of response to initial infection and what are their timescales?

A
  • Innate immunity: 0-4 hours
  • Early induced response: 4-96 hours
  • Adaptive immune response: >96 hours
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2
Q

What happens in 0-4 hours of infection?

A
  • Innate immunity
  • Recognition of infection by nonspecific effectors
  • Removal of the infectious agent
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3
Q

What happens in 4-96 hours of infection?

A
  • Early induced response
  • Recruitment of effect cells
  • Recognition and activation of effector cells
  • Removal of infectious agent
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4
Q

What happens after 96 hours of infection?

A
  • Adaptive immune response?
  • Transport of antigen to lymphoid organs
  • Recognition by naive B and T cells • Clonal expansion of effector cells
  • Removal of infectious agent
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5
Q

What are the mechanical barriers to infection?

A
  • Tight junctions between cells prevent access
  • Air and fluid flow across the epithelium
  • Movement of mucus by cilia
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6
Q

What are the chemical barriers to infection?

A
  • Fatty acids on the skin
  • Enzymes: lysozyme in saliva, sweat and tears
  • Low pH in stomach
  • Antibacterial peptides: defensins (skin and gut) and cryptidins (gut)
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7
Q

what are the microbiological barriers to infection?

A
  • normal flora compete for nutrients and attachment (biofilms)
  • Normal flora produce antibacterial substances (colicins)
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8
Q

What types of cells ingest micro-organisms once across the epithelial barrier?

A
  • Mononuclear phagocytes
  • Macrophages
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9
Q

What receptors recognise microorganisms for ingestion?

A
  • Mannose receptor
  • Glucan receptor
  • Scavenger receptor
  • CD14 (LPS)
  • CD11v/CD18 (CR3)
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10
Q

Describe the environment of a phagosome

A
  • pH of 3-4
  • Toxic oxygen derived products: superoxide, hydrogen peroxide, hydroxyl radical
  • Toxic nitrogen oxides: nitric oxide
  • Peptides: defensins and other cationic proteins
  • Enzymes: lysozyme, acid hydrolases
  • Competitors: lactoferrin, vitamin B12 binding protein
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11
Q

What are the two pathways for bone marrow relating to the immune response?

A

Myeloid:

  • Polymorphonuclear leukocytes
  • neutrophils, basophils, eosinophils

Common lymphoid progenitor:

  • B cells
  • T cells
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12
Q

What are the effects of IFN alpha and beta?

A
  • Induce resistance to viral replication in all cells
  • Increases MHC class 1 expression and antigen presentation in all cells
  • Activation of NK cells to kill virus infected cells
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13
Q

Why are natural killer cells important at the start of the immune response?

A
  • Not specific
  • Don’t require a lengthy clonal expansion of T cells in lymph nodes
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14
Q

What dictates if a natural killer cell is active?

A
  • Balance between signals
  • A positive signal to kill can be overridden by a negative signal by MHC molecules (inhibitory)
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15
Q

What is the complement system?

A

A cascade of serum proteins in the bloodstream

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16
Q

What are the 3 ways of triggering the complement cascade?

A

1) Classical Pathway: Antibody binds to a specific antigen on the pathogen surface
2) Lectin pathway; Mannose-binding protein binds to the pathogen surface
3) Alternative pathway: Pathogen surface creates environment conducive to complement activation

17
Q

What does the activation of the complement cascade lead to?

A
  • Recruitment of mediators of inflammation, phagocyte recruitment
  • Opsonization of pathogens, facilitating uptake and killing by phagocytic cells
  • Lysis and death of pathogens
18
Q

What is C3b?

A

An opsonin

19
Q

What is C3a?

A

Peptide mediator of inflammation

20
Q

What is C5a?

A

Peptide mediator of inflammation

21
Q

Describe how the classical pathway of the complement system is initiated

A

By C1r C3 splits into C3a, which floats away and is a mediator of inflammation, and C3b which acts as an opsonin

22
Q

How is the alternative pathway of the complement system initiated?

A

The spontaneous hydrolysis of serum C3 Triggered by something on the bacterial surface

23
Q

What forms MAC and what does it do?

A
  • C5b, C6 and C7
  • Self assembly
  • Punctures a hole in the surface of the bacteria causing the inner contents to leak out
  • Direct lysis of the bacteria
24
Q

What regulates complement activity?

A
  • DAF: Decay accelerating factor
  • MCP: membrane cofactor protein
  • CR 1: Complement receptor 1
25
Q

Sepsis

A

Complement proteins rise, C3

26
Q

What prevents MAC from attacking the body’s cells?

A

CD59 prevents the parts forming together

27
Q

What is this cell and what is its role?

A

Macrophage

  • Phagocytic cell
  • Circulates in the blood
  • Differentiates into macrophages in tissues
28
Q

What is this cell and what is its role?

A

Macrophage

  • Phagocytic cell
  • Activation of T cells
  • Inititates immune response
29
Q

What is this cell and what is its role?

A

Neutrophil

  • Phagocytic cell (rapidly phagocytoses then dies)
  • Most numerous white blood cell
  • Important in innate immunity
30
Q

What is this cell and what is its role?

A

Eosinophil

  • Killing of antibodies, coated in parasites
  • Releases contents:
  • histamine
  • Peroxidases
  • RNases and DNases
  • Lipases
  • Plasminogen
  • Major basic protein
31
Q

What is this cell and what is its role?

A

Basophil

  • Granulocyte
  • 0.1% of all white blood cells
  • Secretes histamine, proteoglycans, leucotrienes
32
Q

What is this cell and what is its role?

A

Mast cell

  • Release number of substances that effect vascular systems e.g. histamine
  • IgE mediated triggering allergies
33
Q

How long can neutrophils survive for?

A

Circulate for around 12 hours, can survive in tissues for 2 days

34
Q

Neutropenia

A

Low numbers of neutrophils, genetic or as a result of medication e.g. chemotherapy

35
Q

Alpha-1-antitrypsin deficiency

A

Elastase from neutrophils not adequately inhibited

Results in excessive tissue damage during inflammation-pulmonary emphysema

36
Q

How long can eosinophils survive for?

A

Circulate for 12 hours, survive in tissues for 3 days

37
Q

Eosinopenia

A

Seen when glutocorticoids are used

38
Q

In which diseases is Eosinophilia seen?

A

increase

  • Hodgkin’s disease
  • Addison’s disease