Flashcards in B4 Innate vs. Adaptive Immunity Deck (103):
What is the difference between antigens and immunogens?
Antigens - anything that can bind to an antibody.
Immunogens- anything that can illicit an immune response after binding to an antibody.
What is the difference between different epitope structures in antibodies?
What is 'Fab' on antibody molecular models?
Combination of light chains
What is 'Fc' on antibody molecular models?
Combination of heavy chains
What is affinity of antibodies?
How good the binding site is for binding antigens
What is avidity of antibodies?
How much more effectively you bind things with more receptors
Why is there a hinge in the structure of antibodies?
To change and give extreme flexibility of the structure
What are the four ways that allow for an infinite number of different antibodies?
Germ line diversity of genes
What are the components of somatic recombination?
When does somatic hypermutation occur?
During an ongoing immune response
What is somatic recombination?
Joining together lots of different portions of genes that we already have in different orders
What is the term for changing the function of antibody when it gets to the site of infection and realises it has to do something else?
What allows for class switching?
Why does clonal selection exist?
We can't afford to have one gene for each antibody
True or false? Cytokines can induce class switching?
What is positive selection?
If you pass each checkpoint, you survive and divide.
What is negative selection?
If you fail a check point you get killed off.
How many T cells die in the thymus via negative selection?
True or false? B cells and T cells recognise the same part of the antigen?
B cells use Ab
T cells use TCR
How do B cells recognise antigens?
Ab to recognise their complementary conformational epitopes
How do T cells recognise antigens?
TCR to recognise linear epitopes or enzymatically digested bits from B cell antigen processing
What is central tolerance?
How newly developing T cells and B cells are rendered non-reactive to self
What is the purpose of MHC molecules?
To identify small fragments of antigens and shuttle them out to the surface
What is co-stimulation?
Adding another checkpoint for B lymphocytes
Why is co-stimulation necessary?
This ensures that when a B cell phagocytoses something, it doesn't immediately get to make antibodies for it.
What signals do highly immunosuppressive drugs block?
BCR and TCR
What triggers co-stimulation?
Innate system fine discrimination
What are the four steps of the infection pathway?
1. Infection has to establish in face of innate response
2. Induction of adaptive response
3. Reduce/sterilise infection
4. Immunological memory
What type of cell is the effector cell of the dermis?
What protein is responsible for opsinization?
What is the role of C3b?
Recruitment of inflammatory cells
What is MAC?
Membrane Attack Complex
How does MAC work?
Forms perforations in cell membrane resulting in cell lysis
What is degradation?
Breaking down the whole pathogen/antigen into genetic fragments
What is diapedeis?
Movement of while blood cells through intact capillary walls into surrounding tissue.
What is another term for diapedesis?
What are dendritic cells?
Very specialised phagocytes that can return to lymph nodes with information about infections
What are Langerhan cells?
APCs/ Dendritic cells of skin and mucosa
What do Langerhan cells contain?
Where are Langerhan cells most abundant in the skin?
What is the role of dendritic cells?
Turn on T cell responses
Sense the environment
Make a range of cytokines to influence T cell differentiation
What class of MHC molecules do dendritic cells have?
What are high endothelial venues?
Specialised blood vessels for lymphocyte migration
How are high endothelial venules generally used by lymphocytes?
Bloodstream -> Lymph nodes
What kind of signalling do immune cells use?
Similar to synaptic
What happens to T lymphocytes in the process of trapping?
Moved from lymph to bloodstream
What is the difference between TH1 and TH2 CD4 T cells?
TH1 bind to macrophages to make more macrophages
TH2 bind to B cells turned APCs to check them/allow them to make antibodies
What are the cardinal signs of inflammation?
Heat, Redness, Pain, Swelling
Why do the cardinal signs of inflammation come about?
Acute vasodilation of capillaries
What are examples of chronic infections?
Autoimmunity and transplant rejection
What is a major source of mediators for the immune response?
Why are lipids rapidly synthesised?
They're not dependent on protein synthesis
True or false? Cytokines aren't usually dependent on protein synthesis?
What is the specific mechanism of action for dendritic cells?
Where are mast cells usually located?
Next to the vasculature
How are prostaglandins made?
Conversion of arachadonic acid to cyclic endoperoxides which get converted into prostaglandins
How are leukotrienes made?
Conversion of arachadonic acid into 5-lipoxygenase
What are the mediators that resolve inflammation known as?
How are lipoxins made?
Conversion of arachidonate into 15-lipoxygenase
What are leukotrienes?
Biologically active compounds made by leukocytes
What are the 3 As of NSAIDs?
Why isn't paracetamol an NSAID?
It isn't an anti-inflammatory
What does aspirin do to COX?
Inactivates both isoforms
What part of aspirin's actions is responsible for its 3As?
Acetylates catalytic serine residue on position 529
On what levels does aspirin affect COX 2 expression?
Transcriptional and post-transcriptional
How does aspirin end up producing lipoxins?
COX 2 acetylation modifies the enzyme so that instead of completing its reaction to make prostaglandins it stops at lipoxins.
Which mediators are preformed in secretory granules?
What are the mediators of acute inflammations that are newly synthesised?
Activated oxygen species
What are the side effects associated with chronic use of aspirin?
Swelling of eyes, face, lips, tongue or throat
Loss of hearing
Cold clammy skin
True or false? Swelling of the eyes can occur with chronic aspirin use?
Is dry cough a side effect of chronic aspirin use?
What are coxibs?
Selective COX 2 Inhibitors
What are coxibs used for?
What is a famous example of a coxib?
What are NO-NSAIDs?
Nitric oxide -donating NSAID
What are SAIDs?
What does chronic use of corticosteroids cause?
How do mast cells release histamine?
What is the Lewis Triple Response (LTR)?
Reddening, Weal and Flare
Why does the Lewis Triple Response occur?
What is the reddening in LTR caused by?
Vasodilation of small arterioles and pre-capillary vessels
What is wheal in LTR caused by?
Increased permeability of post-capillary venules
What is wheal in the Lewis Triple Response?
Swelling/ Localised oedma
What is flare in the Lewis Triple Response?
Redness extending beyond where you put the foreign object
What is flare in LTR caused by?
Release of vasodilators caused by antidromic stimulation of local nerves
What is the effect of mast-cell activation and granule release on the GI tract?
Increased fluid secretion and peristalsis -> Expulsion of GI tract contents
What is the effect of mast-cell secretion on the eyes, nasal passages and airways?
Decreased diameter and increased mucus secretion -> Congestion and coughing
What is the effect of mast-cell secretion on blood vessels?
Increased blood flow and permeability (potentially -> via anaphylaxis)
What is immediately released by mast-cells on exposure to infection?
Granules containing histamine
What can immediate secretions from mast cells cause?
What can the secretions released by mast cells (after a few minutes of infection) cause?
Recruitment of lymphocytes like neutrophils
What can the secretions released by mast cells (after a few hours of infection) cause?
Class switching from IgG to IgE
What is released by mast-cells after a few minutes of infection exposure?
What is released by mast-cells after a few hours of infection exposure?
What are the effects of histamine after being released from mast cells?
-Increasing vascular permeability
What are the effects of leukotrienes after being released from mast cells?
-Increasing vascular permeability
What are the effects of prostaglandins after being released from mast cells?
-Increasing vascular permeability
What are the effects of TNF alpha after being released from mast cells?
What are the effects of proteases after being released from mast cells?
What is the only mast cell secretion responsible for mucus production?
What is the only mast cell secretion responsible for cell recruitment?
What is the only mast cell secretion responsible for chemotaxis?