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PCS 2 > Immunity > Flashcards

Immunity Flashcards

1
Q

Saprophytic

A

x

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2
Q

Commensal

A

Organsims living in another without causing injury/ damage to host
Benefit the host

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3
Q

Pathogen

A

Disease causing organism/ agent

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4
Q

Opportunist

A

x

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5
Q

Infection that is acquired form ones own flora

A

Endogenous

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6
Q

Infection that is acquired form another source

A

Exogenous

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7
Q

Other name for innate immunity

A

Natural

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8
Q

Other name for adaptive immunity

A

Acquired

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9
Q

Complement System

A
  1. A complement factor from plasma binds to a bacterium
  2. This attracts other complement factors that form a hole in the cell membrane called the Membrane Attack Complex (MAC)
  3. In the process smaller complement components are released called anaphylatoxins. These attract phagocytic cells
  4. The phagocyte engulfs and then destroys the bacterium
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10
Q

What are the 2 different responses of adaptive immunity?

A

Humoral & cell-mediated

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11
Q

Which cells are involved with the humoral response?

A

B lymphocytes
Plasma cells
Memory cells
Antibodies

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12
Q

Which cells are involved with the cell-mediated response?

A

T lymphocytes
T helper cells
Cytotoxic T cells

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13
Q

Describe the clonal selection theory

A
  1. A B lymphocyte binds to a bacterium via its surface antibody which specifically recognises a site (epitope) on the bacterial surface
  2. The bacterium is ingested
  3. A fragment of the bacterium is displayed on the B cell surface
  4. This attracts a T helper cell which also recognises this fragment
  5. As a result cytokines are released from the T cell
  6. This causes proliferation of the B cells and T cells forming colonies of identical cells
  7. The colony of B cells mature into plasma cells that are able to secrete antibody. These antibodies are identical in structure to the original surface antibody on the naive B cell i.e they have the same specificity for antigen
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14
Q

What’s another word for antibody?

A

Immunoglobulin

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15
Q

Describe sequences of a viral infection

A
  1. A virus hides inside a cell
  2. A fragment of the virus is displayed on the cell surface
  3. This attracts cytotoxic T cells and cytokines are released from the T cells
  4. The cytokines cause the death of the infected cell and proliferation of a colony of identical T cells
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16
Q

Name for secreted proteins that attract cells bearing chemokine receptors out of the bloodstream into affected tissue

A

Chemokines

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17
Q

Elements of innate immunity

A

Anatomical barriers (skin/ mucous membrane)
Physiological barrier (temp/ pH/ chemicals)
Phagocytic
Inflammatory
Complement

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18
Q

Which antibody is present in saliva?

A

IgA

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19
Q

Can opportunists arise from saprophytic/ commensal/ pathogenic organisms?

A

Yes

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20
Q

When may aprophytic/ commensal/ pathogenic organisms become opportunists?

A 
If immunocompromised 
Wound
Catheter 
Antacids 
Antibiotic
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21
Q

What are anaerobes and when could they cause disease?

A

They lack oxidative enzymes so rely on fermentative processes (producing smelly volatile gases)
Killed by oxygen so can survive and cause disease in low oxygen environments e.g. large bowel/ dental crevices

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22
Q

Illnesses associated with Streptococci?

A

Otitis media
Pneumonia
Meningitis
Septicaemia

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23
Q

Name a virulance factor of Strep pneumoniae and Staph aureus

A

Capsule

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24
Q

What does the purple staining of gram + bacteria show the presence of?

A

Peptidoglycan layer

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25
Q

What kind of stain does gram - bacteria show?

A

Red counterstain

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26
Q

Difference between gram + and - bacteria

A

+ Thick peptidoglycan layer, no outer membrane

- Thin peptidoglycan layer and outer membrane

27
Q

Direct strep infections

A

Tonsillitis
Cellulitis sepsis
Pneumonia

28
Q

Toxin mediated strep infections

A

Scarlet fever
Toxic sock syndrome
Necrotizing fasciitis

29
Q

Late immunological sequele strep infections

A

Rheumatic fever
Glomerulonephritis
Henloch Schonlein purpura
Erythema nodosum

30
Q

What is the difference between the 90 serotypes of S pneumonia?

A

Different capsular polysaccharides

31
Q

Serious disease often caused by pneumococci?

A

Pneumonia
Meningitis
Febrile bacteraemia

32
Q

Common and less serious disease often caused by pneumococci?

A

Otitis media
Sinusitis
Bronchitis

33
Q

3 ways an extracellular polysaccharide capsule increases the virulence of a microbe

A
  1. Capsule prevents opsonisation by complement/ antibodies
  2. Capsule is hydrophilic that hinders its uptake by phagocytosis
  3. Capsules are weakly immunogenic - mimic host structures to be seen as a self antigen
34
Q

What family does the Ebola virus belong to?

A

Filoviridae

35
Q

What Baltimore group does Ebola belong to?

A

Group 5

- single stranded RNA

36
Q

Cells that express Toll-like receptors

A 
Phagocytic macrophages
Dendritic cells 
B cells 
Natural killer cells 
Certain epithelial cells
37
Q

What is always the 1st antibody generated?

And 2nd?

A

IgM

then IgG1

38
Q

How do immunoglobulins have such diversity in antigen recognition?

A

Rearrangement of DNA in variable region

39
Q

What can T cell receptors recognise?

A

MHC I proteins

Peptide derived proteins of pathogens

40
Q

What do MHC class I protein present peptides to?

A

CD8 T

41
Q

What do MHC class II protein present peptides to?

A

CD4 T

42
Q

What activates the Classical Pathway of the complement system?

A

Antibodies (principally IgM and IgG)

C-reactive protein bound to bacteria/ apoptotic cells

43
Q

What does C1q do?

A

1st component of complement system

Recognises:
IgM and IgG (antibodies)
C1r and C1s (serine proteases)

Binds to antibodies only if antibody if bound to its antigen
Several C1q can bind to IgM - causes a conformational change in C1q
Causing activation of C1r and initiation of classical pathway
Binds to IgG but is less efficient as IgG is a monomer

44
Q

How many Ig molecules does IgM contain?

A

5 (M for mega)

45
Q

How is lectin pathway activated?

A

Mannose binding lectin (MBL) binds to mannose residues on pathogen
or
Ficollin binds to N-acetyl glucosamine on pathogens

46
Q

What does activation of C1r, C1s and MASPs cause?

A

Activation and cleavage of C4 into C4a and C4b

And subsequent activation of C2 into C2a and C2b

47
Q

What does C2b do?

A

Activates C3 to form C3a and C3b

48
Q

Which pathway in the complement system is considered an amplification pathway?

A

The alternative pathway

49
Q

What do all 3 pathways of the complement system lead to?

A

Cleavage of C3 into C3a and C3b

50
Q

What is meant by C3b/C4b fixation (opsonisation)?

A

C3b and C4b get fixed to pathogens and immune complexes

So they are recognised by phagocytes

51
Q

What is C3b opsonised on bacteria recognised by?

A

CR3 e.g. on surface of neutrophils

52
Q

What is C3b opsonised on immune complexes recognised by?

A

CR1 on erythrocytes

53
Q

Consequence of C1 and C4 deficiency?

A

Impaired immune handling

Associated with SLE (lupus)

54
Q

What is C5b?

A

1st molecule of membrane attack complex

55
Q

What is C5a?

A

Important chemotactic agent for neutrophils/ monocytes/ macrophages
Or can directly activate neutrophils and enhance their ability to phagocytose bacteria

56
Q

What can excess C5a cause?

A

Pro-inflammatory

Rheumatoid arthritis

57
Q

What properties do anaphylatoxins have?

A

Vasodilation

Bronchoconstriction

58
Q

What extrinsically regulates the complement system?

A

C1-inhibior

59
Q

What intrinsically regulates the complement system?

A

IgM and IgG must undergo conformational change before C1 can bind
Enzymes circulate as zymogens
Thiol group only becomes available when C3 and C4 are enzymatically cleaved/ activated

60
Q

How does TNFa promote extravasation (leakage) of neutrophils?

A

By:

a) increasing the permeability of local endothelium
b) up regulating adhesion receptors (selectins) on the surface of the endothelium

local release of TNFa in an infection is good, systemic release of TNFa in sepsis is life-threatening

61
Q

Which Toll-like receptor is activated when exposed to double stranded RNA?

A

TLR3

62
Q

Consequence of Neisseria gonorrhoeae and Neisseria meningitidis producing a protease capable of cleaving IgA molecules?

A

Impaired mucosal immune protection

63
Q

Arrange mast cell/ eosinophil/ basophil in order of
1) main leukocyte mediate
2) next most important
3) next most important
in an allergic response/ type I hypersensitivity

A

Mast cell
Eosinophil (eosinophils are more abundant in number than basophils)
Basophil

allergic response mediated by IgE already pre-bound to the Fc epsilon receptor found on basophils and eosinophils

64
Q

IgA is the antibody isotype found in the greatest concentrations in breast milk because IgA can exist as a dimer whereby the dimer can be recognised by the poly-Ig receptor that facilitates the secretion of polymeric antibodies.

Just to confirm, whereas IgM, IgG and monomeric IgA are adapted to provide protection within fluids and tissues of the body, dimeric IgA protects the surfaces of the mucosal epithelia including the linings of the urinary and genital tracts. IgA protects primarily by neutralising the pathogen. However, secretory IgA has little capacity to activate complement or to act as an opsin.

Note that IgM and IgG3 are the major antibody isotypes associated with the classical pathway of complement activation. IgM is ideally suited to the task because of its pentameric ‘staple’ conformation when bound to the surface of a pathogen. With this form of IgM, the individual Fc regions (x5) can readily bind to complement factor, C1q, that requires multipoint attachment for stable binding. So even though IgM is a low-affinity antibody it is very good at activating complement. As IgG exists as a monomer, it is necessary for C1q to cross-link two or more IgG molecules in order to obtain multipoint attachment and stable binding. Consequently, the activation of complement by IgG is very dependent upon high antibody density on the surface of the pathogen.
IgA1 and IgA2 are also capable of activating complement but not nearly as effectively as IgM and IgG.

IgG is present at higher levels in the serum than other isotypes because of its versatility and capacity to enter extracellular spaces in tissues. IgG is very efficient at promoting phagocytosis because it acts as an opsonin, coating the pathogen and allowing recognition by Fcgamma receptors on our phagocytes. IgGs are also very efficient at neutralisation.

We still know very little about the functional roles of IgD

Remember that the normal physiological role of IgE is to counter parasites by binding to surface of parasite and thereby recruiting eosinophils, basophils and mast cells that possess the high affinity Fc epsilon receptor that binds to IgE. In fact, the affinity of IgE for the Fcepsilon R is so high that most IgE is already bound to the receptor in the absence of antigen. Exposure to antigen leads to cross-linking of Fcepsilon receptors and degranulation of eosinophils, basophils and mast cells.

A

c

PCS 2 (8 decks)

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