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204: The immune system > Innate immunity 1 > Flashcards

Innate immunity 1 Flashcards

1
Q

What is innate immunity?

A

1st line of defence against infection

Present at birth and passed down genetically

Occurs within minutes of pathogen recognition

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2
Q

Characteristics of innate immunity

A

Specificity inherited in the genome

Triggers immediate response

Recognises broad classes of pathogens

Interacts with a range of molecular structures of a given type

Able to discriminate between even closely related molecular structures

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3
Q

Innate barriers to infection

A

Physical

  • skin
  • GI tract
  • respiratory tract

Soluble

  • complement
  • defensins
  • collectins

Induced

  • innate immune cells
  • pattern recognition receptors
  • interferon
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4
Q

Tissue damage

A

Causes release of vasoactive and chemoactic factors that trigger local increase in blood flow and capillary permeability

Permeable capillaries allow influx of fluid and cells

Phagocytes migrate to site of inflammation

Phagocytes and antibacterial exudates destroy bacteria

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5
Q

Soluble innate immune molecules

A

Enzymes such as lysozyme- disrupt bacterial cells walls, found in blood and tears

Antimicrobial peptides- disrupt microbial membranes

Collectins, ficolins and pentraxins- bind to pathogens targeting them for phagocytosis and activate complement

Complement components- lyse bacteria, opsonise bacteria, induce inflammation

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6
Q

Lysozyme

A

Secreted by phagocytes and paneth cells fro the small intestine

Most effective against gram positive bacteria

Cleaves the bond between the alternating sugars that make up peptidoglycans

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7
Q

Antimicrobial peptides

A

Cover epithelial surfaces, found in saliva

Constitutively secreted by neutrophils, epithelial cells and paneth cells in the crypts of the small intestine

Kill bacteria in minutes, by disrupting the membrane

Attack fungi, viruses

Inhibit DNA and RNA synthesis

e.g. histatins, defensins, cathelicidins

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8
Q

Histatins

A

Produced in the oral cavity

Active against pathogenic fungi e.g. candida albicans

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9
Q

Cathelicidins

A

LL-377 broad spectrum antimicrobial activity

Against both gram negative and gram positive bacteria

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10
Q

Defensins

A

Two classes- alpha, beta

35-40 aa amphipathic peptides

Disulphide bonds stabilise the structure to have a positively charged region separated from a hydrophobic region

Disrupt microbial membranes but not that of the host

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11
Q

Collectins

A

Globular lectin like heads that bind to bacterial cell surface sugars

Sialic acid hides mannose antigens on host cells

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12
Q

Ficolins

A

Recognises acylated compounds such as n acetylglucosamine, a monosaccharide found in bacterial cell walls

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13
Q

Pentraxins

A

Cyclic multimeric proteins found in the plasma

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14
Q

Actions of collectins, ficolins and pentraxins

A

Soluble pattern recognition receptors

Act as opsonins that bind to pathogens and infected cells targeting them for phagocytosis

Activate complement through the classical pathway/ lectin pathway

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15
Q

3 complement pathways

A

Classical pathway

Lectin pathway

Alternative pathway

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16
Q

Complement system

A

Series of over 30 proteins constantly circulate in blood and fluids that bathe the body tissues

When they detect presence of foreign material, they initiate a cascade of reactions that amplify the signal

When activated, cooperate with other host defence systems to generate inflammation and rapidly remove the pathogen

Most made by the liver, also produced by monocytes, macrophages and epithelial cells of the intestine and urinary tract

17
Q

Complement components

A

Circulate as pro-form in the blood

Numbered in the order they were discovered, not in the order they are activated

Some have proteolytic enzymatic activity

On activation they split into a small and large framents triggering an amplification cascade

18
Q

Effects mediated by complement components

A

Lysis

Opsonisation

Activation of inflammatory response

Clearance of immune complexes

19
Q

Classical pathway

A

Initiated by C1 activation

C1 is a complex of three proteins: C1q, C1r and C1s

The structure of C1 is dominated by C1q

  • large molecule of 18 polypeptides
  • form 6 collagen like triple helix structures
20
Q

Classical pathway: activation

A

Triggered when C1 binds to the Fc region of an antibody- antigen complex

C1 must bind at least 2 Fc domains

Causes conformational change in C1r

C1s cleaved and can activate C2 and C4 splitting

C3 convertase activate over 200 C3 molecules- amplification

C4b, C2a and C3b fragments form C5 convertase that activates C5 leading to membrane attack complex

21
Q

Serum IgM

A

Cannot bind C1 as it has a planar conformation

Shape changes on binding antigen to reveal binding sites for C1q

22
Q

IgM

A

Most efficient at activating complement

Has 5 Fc domains

23
Q

Lactin pathway

A

Antibody independent, activated by ficolins and mannose binding lectin

BML binds mannose residues on carbohydrates and glycoproteins on bacteria and some viruses

Similar downstream mechanism to classical pathways

Upon binding BML forms a complex with MASP-1 and MASP-2 (serine proteases)

Active complex cleaves C2 and C4

24
Q

Alternative pathway

A

C3 spontaneous hydrolysis into C3a and C3b

C3b binds to cell membrane and factor B, making it susceptible to cleavage by factor D to Bb

C3bBb has half life of 5 minutes, unless it binds to serum protein properdin, which extends its half life to 30 minutes protecting it from proteases

C3bBb can hydrolyse more C3 creating more C3b which can amplify the signal

25
Q

Membrane attack complex

A

MAC forms a pore that inserts into the membrane

Allows diffusion of ions and small molecules

Water moves into the cell killing it

Human cells have soluble and cell surface associated proteins that prevent MAC formation

26
Q

Complement inhibitors

A

C1 inhibitor: soluble protein that prevents C1 activating C4 and C2

Series of soluble and membrane bound inhibitors prevent C3 activation, especially in alternative pathway

Membrane bound inhibitors prevent action of the membrane attack complex

27
Q

Heriditary angioedema

A

C1 inhibitor deficiency

Classical complement cascade easily activated

Can be easily treated with an injection of C1 inhibitor

28
Q

Complement deficiency

A

Deficient of components of complement pathway experience recurrent infections

MBL deficiency causes serious pyogenic infections in neonates and children

C3 deficiency is the most severe leading to successive severe infections

Patients deficient of C8 are prone to infections with Neisseria meningitis

29
Q

SLE

A

Systemic lupus erythematosus

30
Q

COmplement deficiency in SLE

A

90% people deficient for C4 develop SLE

C4 deficiency means less C3b (C4b2a is C3 convertase)

C3b bound to immune complexes binds to Cr1 on erythrocytes which transports them to phagocytes in the liver and spleen

Phagoyctes recognise the immune complexes via their Fc receptors and engulf them

204: The immune system (19 decks)

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