Innate immunity 1 Flashcards

1
Q

Key characteristics of the innate immune system [6]

A

Genome encoded

Some receptors are expressed by all cells of a cell type
- Like in macrophages.

Immediate response.

Not specific to antigens.
-	Recognizes broad class of antigens using PRRs.

Interacts with a range of molecular structures of a given type.

Able to discriminate between closely related molecular structures.
- As seen with MBL.

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2
Q

Mechanical anatomical barriers against pathogens [4]

A

Tight junctions in epithelial cells: skin, gut, eyes, nose, mouth, lungs.

Longitudinal flow of air/fluid: gut, skin.

Movement of mucus by cilia: lungs.

Tears and nasal cilia: eyes, nose, mouth.

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3
Q

Chemical anatomical barriers against pathogens [5]

A

All structures: antimicrobial peptides.

Skin: Fatty acids

Gut: Low pH, antimicrobial peptides.

Lungs: Pulmonary surfactant containing collectins.

Eyes, nose, mouth: Antimicrobial enzymes in tears and saliva.

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4
Q

Microbiological anatomical barriers against pathogens

A

Normal microbiota in all structures (skin, lungs, eyes, nose, gut, mouth)

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5
Q

Pentraxins

A

Soluble molecule- cyclic multimeric protein

Binds to pathogens, tags for phagocytosis.

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6
Q

Lysoszyme

A

Antimicrobial enzyme

  • Found in tears, saliva
  • Dirupts bacterial cells walls
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7
Q

Phospholipase A2

A

Secretory form acts as antimicrobial enzyme

  • Found in the blood
  • Disrupts bacterial cell wall
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8
Q

Antimicrobial peptides [4]

A

Amino acid chains secreted by neutrophils, paneth cells (small intestines)
- Cover epithelial surfaces, found in saliva.

  • Disrupts bacterial membrane.
  • Attacks fungi and viruses.
  • Inhibits RNA and DNA synthesis.
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9
Q

Histatins

A

Antimicrobial peptide

  • Produced in oral cavity
  • Attacks fungi, like c. abicans
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10
Q

Defensins

A

Amphipathic, antimicrobial peptide that disrupt microbial cell membranes by forming a pore in plasma membrane
- Does not attack host cells

Structure

  • 35-40 a.a
  • Disulphide bonds to stabilise structure
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11
Q

Collectins

A

Pattern recognition receptor

  • Lectin head binds to sugars on bacterial surface
  • Collagen tail binds to phagocytes

Example: MBL, activates complement cascade
- Host cells are protected via sialic acid covering mannose

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12
Q

Ficolins

A

Trimer molecule that recognises acylated compounds on bacterial cell wall
- Collagen and fibrinogen domain

  • Activates complement
  • Carries out opsonisation
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13
Q

Action of ficolins, collectins and pentaxins.

A

Act as soluble PRR

Opsonisation of infected cells for phagocytosis

Activation of the classical/ lectin complement pathway.

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14
Q

Classical component pathway

- Activation

A

Activated by Ag-Ab complex binding to C1q on C1qC1rC1s.
- IgM is usually the antigen, and at least 2 Fc domain bound to C1q.

IgM can only bind in staple form, not planar
- Staple form occurs when bound to Ag.

Activated C1q cleaves C14.

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15
Q

Classical component pathway

- Amplification

A

Activated C1r cleaves C1s
- C1s cleaves C2 and C4

C2a and C4b form C3 convertase
- Cleaves C3 into C3a, C3b.

C3b, C2a, C4b combine to form C5 convertase
- Cleaves C5, forms membrane attack complex (MAC)

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16
Q

Lectin component pathway

- Activation

A

Activated by MBL or ficolin bound to pathogen

- MBL forms complex with MASP1, 2.

17
Q

Lectin component pathway

- Amplification

A

MBL-MASP1/2 complex cleaves C2, C4

- Forms C3/5 convertase leaving to C3b and MAC production downstream

18
Q

Alternative component pathway

- Activation

A

Pathogenic surface comes into contact with C3

- Spontaneous lysis into 3a, 3b.

19
Q

Alternative component pathway

- Amplification

A

C3b binds to cell membrane/ factor B
- Cleaves Factor D into Bb.

C3bBb can cleave C3, making more C3b

C3bBb only has a half life of 5 mins
- Prolonged by the release of properdin from leucocytes during inflammation.

20
Q

C3a, C5a function

A

Peptide mediator of inflammation

Recruits phagocytes

21
Q

C3b function

A

Opsonisation

- Binds to complement receptor on phagocyte- facilitate phagocytosis to remove immune complexes

22
Q

MAC

A

Membrane attack complex
- Formed from the activation form C6 by C5b—> cascade to from C5b6789

MAC forms pores in cell membrane
- Influx of water, ions, sugar= cell lysis

Host cells protected against MACs via soluble and cell surface proteins

23
Q

Hereditary angioedema

A

Caused by C1 inhibitor deficiency
- Leads to easy activation of Classical complement cascade

Symptoms
- Swelling in hands, face, feet and airway

24
Q

MBL deficiency

A

Inhibits Lectin complement pathway
- Leads to severe pyogenic infections in children and neonates

Eventually recovers with age due to compensation from adaptive immune system

25
Q

C3 deficiency

A

Prevents the formation of C3b in all complement pathways

- Most severe due to the important role of C3b (cannot opsonise bacteria)

26
Q

C8 deficiency

A

Associated with being prone to meningitis infection (Neissera)

27
Q

SLE and complements

A

90% of those with C4 deficiency develop SLE
- Inability to make C3 convertase, hence C3b

C3b cannot bind to CR1 on rbc- not transported to phagocytes in liver/spleen- immune complexes not removed via phagocytosis

28
Q

Roles of activated complements

A
  • Creation of membrane attack complex (C5-9)= pores in microbial cell membrane
  • Opsonisation (C3b)
  • Chemoattractant for leucocytes