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PCS > Unit 2 - Principles of immunology > Flashcards

Unit 2 - Principles of immunology Flashcards

1
Q

describe the metabolism of bacteria

A

facultative: anaerobic - does not have detoxification enzymes - slower process - yields 47 kCal/ aerobic - yields 487 kCal

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2
Q

describe the two types of bacteria according to their cell wall

A

gram positive -thick wall of peptidoglycan - stains purple
gram negative - double membrane - peptidoglycan and lipopolysaccharide - negative charge - does not stain but with counter stain - pink

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3
Q

how can bacteria be identified?

A
  • colony morphology - coccus (round)/ bacillus (rod)/ spirillus/ spirochaetes (helix)
  • microscopy
  • substances produced
  • growth requirement
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4
Q

describe properties of fungi

A
  • eukaryotic in nature
  • unicellular or multicellular
  • molds form mycelia - hyphae
  • cell wall made of chitin
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5
Q

what type of infection do fungi form?

A
  • superficial

- systemic

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6
Q

how are protozoa classified?

A

according to locomotion = appendages/ pseudopodia (amoeba)

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7
Q

describe properties of protozoa

A
  • eukaryotic
  • unicellular
  • free living or parasite
  • absorb nutrients from environment
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8
Q

describe helminths

A

multicellular parasites

round worms and flat worms

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9
Q

what are prions?

A

misfolded proteins causes TSE (transmissible spongiform encephalopathies) - rare progressive neurodegenerative disorders

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10
Q

describe the structure of viruses

A

capsomeres - capsids
envelope
contain either RNA or DNA

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11
Q

how are viruses detected?

A

serology - antibodies
microscopy
culture
PCR

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12
Q

describe the life cycle of a virus

A

entry- uncoating -replication - protein synthesis - assembly - release

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13
Q

describe types of viral infections

A

acute/ lytic
chronic
latent/ proviral
transformation

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14
Q

what is the baltimore classification of viruses?

A

classification based on nucleic genomes
(+) = sense - used as mRNA directly for translation
(-) = anti-sense - have to produce mRNA
1. dsDNA (herpes)2. ssDNA (adenovirus) 3. dsRNA (neovirus) 4. (+)ssRNA (polio/ hep A/ hep C) 5. (-) ssRNA (influenza) 6. reverse RNA (HIV) 7. reverse DNA (hep B)

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15
Q

what are the two types of infections?

A

endogenous - self-infection

exogenous - person to person transmission/ environmental/ HCA

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16
Q

what are virulence factors?

A

pathogenesis

  • adhesion
  • capsule
  • resistance to serum
  • biofilm
  • motility
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17
Q

where are the most common portals of entry?

A

respiratory tract
GI tract
gastrourinary tract

18
Q

what are commensal flora?

A

micro-organisms that reside in body but do not cause harm - benefit to host (mouth, gut. skin. upper airway)

19
Q

describe the cellular components of innate immunity

A

blood: monocyte/ NK cells/ granulocytes - neutrophils/ eosinophils/ basophils
tissue: macrophage/ mast cells/ dendritic cells/ NK cells

20
Q

what are the functions of the components found in tissue?

A

macrophages - use PRRs to recognise PAMP
mast cells - cause allergic reactions - IgE constant region bound to them when activated degranulates and releases histamines
dendritic cells: activate adaptive immunity
NK cells: attack host cells

21
Q

what are PAMPs and what are they recognised by?

A

PAMP: pathogen associated molecular patterns - compnents of pathogens which distinguish it from host cell
recognised by PRRs -pattern recognition receptors - most common TLRs -toll-like receptors expressed by macrophages/ dendritic cells/ B cells/ NK cells

22
Q

which TLRs are found on plasma membrane- what happens when they are triggered?

A

TLR4, TLR5, TLR1: TLR2, TLR2: TLR6
detect extracellular pathogens - activate transcriptional factor NFkB
- release of cytokines: TNF a/ IL-1/ IL-6
- expression of co-stimulatory receptors: B7-1/ CD80 and B7-2/ CD86

23
Q

which TLRs are found on endosomal compartments?

A

TLR3
TLR7
TLR9

24
Q

what are the key soluble proteins of innate immunity?

A

cytokines
antimicrobial peptides
complement proteins

25
Q

summarise the complement system

A

classical, lectin and alternative pathway lead to the activation of the terminal pathway: C5a induced inflammation and MAC mediated cell lysis

26
Q

explain how the classical and lectin pathways lead to the activation of C3

A

classical: activated when IgM or IgG binds to pathogen- recognised by C1
lectin: activated by mannose residues on pathogen - recognised by MBL (mannan binding lectin)

  • these two pathways converge at activation of C4 which leads to the activation of C3
27
Q

explain the alternative pathway

A

autoactivated C3 leads to the binding of Factor B with C3(H2O)
- factor B is cleaved by factor D to produce C3(H2O)B
which is a convertase cleaving C3 into C3a and C3b

28
Q

what effector function is mediated by C3b?

A

C3b mediated opsonisation - C3b fixed to the pathogen which can be recognised by CR1 or CR3 found on surface of neutrophils to initiate phagocytosis

29
Q

how is the termination pathway activated?

A

after activation of C3 the termination pathway is activated resulting in the cleavage of C5 into C5a and C5b

30
Q

what is the effector function of C5a?

A

C5a - anaphylatoxin

  • attracts neutrophils and marophages to site of infection to induce phagocytosis
  • induces inflammation via vasodilation and bronchoconstriction
31
Q

what is the effector function initiated by C5b ?

A

(membrane attack complex) MAC-mediated cell lysis
= C5b binds to C6 and C7 forming complex C5bC6C7
- complex becomes hydrophobic and binds to membrane
- C8 and multiple C9 molecules bind and form transmembrane pore (MAC/ C5b-9)
- this leads to cell lysis

32
Q

what is the effect of deficiency in components for MAC

A

increased susceptibility to infection - specifically neisseria species

33
Q

describe the basis of inflammation

A

macrophages/mast cells send cytokines

  • triggering innate immune response
  • induces inflammation - vasodilation results in oedema and pain due to pressure on nerves
  • attraction of inflammatory cells increase oedema levels
  • activation of hypothalamus increase body temperature more difficult for replication of pathogens

inflammation deceases when macrophages eliminate dead neutrophils

34
Q

what is the clonal selection hypothesis?

A

shape of antibodies is predetermined due to 3D structure
random nature of generation causes possibility of developing receptors that recognise self antigens so they are clonally deleted
leaves a pool of mature naive lymphocytes and lymphocyte with appropriate receptor for pathogen undergoes clonal expansion = monoclonal antibodies

35
Q

where is adaptive immunity initiated?

A

dendritic cells in the peripheral tissue migrate to lymph nodes along lymphatic vessels where naive T cells are activated

36
Q

describe structure of TCR

A

similar to antibody as it has variable and constant region but it is a transmembrane protein

37
Q

describe how antigen processing and presentation works

A

proteins derived from pathogen are processed into peptide fragments
these fragments bind to major histocompatiblity complex (MHC) receptors which display pathogen on surface of infected cell to be recognised by TCR

38
Q

what is the difference between class I and class II MHC receptors?

A 
class I - expressed on all nucleated cells - recognised by CD8+ T-cells (T-killer cells)
class II - only expressed on professional antigen presenting cells: B cells/ macrophages/ conventional dendritic cells - recognised by CD4+ T-cells
39
Q

how is the diversity of immunoglobulins achieved?

A

somatic rearrangement - different combinations of V domains with D&J domains

40
Q

what are the five classes of immunoglobulins?

A 
IgA -breast milk
IgD
IgE - mast cells
IgG 
IgM - first antibody produced - pentimer
41
Q

what are the mechanisms of action of immunoglobulins?

A

opsonisation
complementation
neutralisation/ agglutination

PCS (29 decks)

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