Immunity Flashcards
(64 cards)
1
Q
Saprophytic
A
x
2
Q
Commensal
A
Organsims living in another without causing injury/ damage to host
Benefit the host
3
Q
Pathogen
A
Disease causing organism/ agent
4
Q
Opportunist
A
x
5
Q
Infection that is acquired form ones own flora
A
Endogenous
6
Q
Infection that is acquired form another source
A
Exogenous
7
Q
Other name for innate immunity
A
Natural
8
Q
Other name for adaptive immunity
A
Acquired
9
Q
Complement System
A
- A complement factor from plasma binds to a bacterium
- This attracts other complement factors that form a hole in the cell membrane called the Membrane Attack Complex (MAC)
- In the process smaller complement components are released called anaphylatoxins. These attract phagocytic cells
- The phagocyte engulfs and then destroys the bacterium
10
Q
What are the 2 different responses of adaptive immunity?
A
Humoral & cell-mediated
11
Q
Which cells are involved with the humoral response?
A
B lymphocytes
Plasma cells
Memory cells
Antibodies
12
Q
Which cells are involved with the cell-mediated response?
A
T lymphocytes
T helper cells
Cytotoxic T cells
13
Q
Describe the clonal selection theory
A
- A B lymphocyte binds to a bacterium via its surface antibody which specifically recognises a site (epitope) on the bacterial surface
- The bacterium is ingested
- A fragment of the bacterium is displayed on the B cell surface
- This attracts a T helper cell which also recognises this fragment
- As a result cytokines are released from the T cell
- This causes proliferation of the B cells and T cells forming colonies of identical cells
- 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
14
Q
What’s another word for antibody?
A
Immunoglobulin
15
Q
Describe sequences of a viral infection
A
- A virus hides inside a cell
- A fragment of the virus is displayed on the cell surface
- This attracts cytotoxic T cells and cytokines are released from the T cells
- The cytokines cause the death of the infected cell and proliferation of a colony of identical T cells
16
Q
Name for secreted proteins that attract cells bearing chemokine receptors out of the bloodstream into affected tissue
A
Chemokines
17
Q
Elements of innate immunity
A
Anatomical barriers (skin/ mucous membrane)
Physiological barrier (temp/ pH/ chemicals)
Phagocytic
Inflammatory
Complement
18
Q
Which antibody is present in saliva?
A
IgA
19
Q
Can opportunists arise from saprophytic/ commensal/ pathogenic organisms?
A
Yes
20
Q
When may aprophytic/ commensal/ pathogenic organisms become opportunists?
A
If immunocompromised Wound Catheter Antacids Antibiotic
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
22
Q
Illnesses associated with Streptococci?
A
Otitis media
Pneumonia
Meningitis
Septicaemia
23
Q
Name a virulance factor of Strep pneumoniae and Staph aureus
A
Capsule
24
Q
What does the purple staining of gram + bacteria show the presence of?
A
Peptidoglycan layer
25
What kind of stain does gram - bacteria show?
Red counterstain
26
Difference between gram + and - bacteria
+ Thick peptidoglycan layer, no outer membrane
| - Thin peptidoglycan layer and outer membrane
27
Direct strep infections
Tonsillitis
Cellulitis sepsis
Pneumonia
28
Toxin mediated strep infections
Scarlet fever
Toxic sock syndrome
Necrotizing fasciitis
29
Late immunological sequele strep infections
Rheumatic fever
Glomerulonephritis
Henloch Schonlein purpura
Erythema nodosum
30
What is the difference between the 90 serotypes of S pneumonia?
Different capsular polysaccharides
31
Serious disease often caused by pneumococci?
Pneumonia
Meningitis
Febrile bacteraemia
32
Common and less serious disease often caused by pneumococci?
Otitis media
Sinusitis
Bronchitis
33
3 ways an extracellular polysaccharide capsule increases the virulence of a microbe
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
What family does the Ebola virus belong to?
Filoviridae
35
What Baltimore group does Ebola belong to?
Group 5
| - single stranded RNA
36
Cells that express Toll-like receptors
```
Phagocytic macrophages
Dendritic cells
B cells
Natural killer cells
Certain epithelial cells
```
37
What is always the 1st antibody generated?
| And 2nd?
IgM
| then IgG1
38
How do immunoglobulins have such diversity in antigen recognition?
Rearrangement of DNA in variable region
39
What can T cell receptors recognise?
MHC I proteins
| Peptide derived proteins of pathogens
40
What do MHC class I protein present peptides to?
CD8 T
41
What do MHC class II protein present peptides to?
CD4 T
42
What activates the Classical Pathway of the complement system?
Antibodies (principally IgM and IgG)
| C-reactive protein bound to bacteria/ apoptotic cells
43
What does C1q do?
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
How many Ig molecules does IgM contain?
5 (M for mega)
45
How is lectin pathway activated?
Mannose binding lectin (MBL) binds to mannose residues on pathogen
or
Ficollin binds to N-acetyl glucosamine on pathogens
46
What does activation of C1r, C1s and MASPs cause?
Activation and cleavage of C4 into C4a and C4b
| And subsequent activation of C2 into C2a and C2b
47
What does C2b do?
Activates C3 to form C3a and C3b
48
Which pathway in the complement system is considered an amplification pathway?
The alternative pathway
49
What do all 3 pathways of the complement system lead to?
Cleavage of C3 into C3a and C3b
50
What is meant by C3b/C4b fixation (opsonisation)?
C3b and C4b get fixed to pathogens and immune complexes
| So they are recognised by phagocytes
51
What is C3b opsonised on bacteria recognised by?
CR3 e.g. on surface of neutrophils
52
What is C3b opsonised on immune complexes recognised by?
CR1 on erythrocytes
53
Consequence of C1 and C4 deficiency?
Impaired immune handling
| Associated with SLE (lupus)
54
What is C5b?
1st molecule of membrane attack complex
55
What is C5a?
Important chemotactic agent for neutrophils/ monocytes/ macrophages
Or can directly activate neutrophils and enhance their ability to phagocytose bacteria
56
What can excess C5a cause?
Pro-inflammatory
| Rheumatoid arthritis
57
What properties do anaphylatoxins have?
Vasodilation
| Bronchoconstriction
58
What extrinsically regulates the complement system?
C1-inhibior
59
What intrinsically regulates the complement system?
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
How does TNFa promote extravasation (leakage) of neutrophils?
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
Which Toll-like receptor is activated when exposed to double stranded RNA?
TLR3
62
Consequence of Neisseria gonorrhoeae and Neisseria meningitidis producing a protease capable of cleaving IgA molecules?
Impaired mucosal immune protection
63
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
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
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.
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