IMMUN: Infection + Immunity Flashcards
1
Q
cytokine storm
A
- occurs during severe COVID
- lots of pro-inflammatory cytokines
- overactive immune system > weakened and susceptible to superinfection
- more tissue damage (producing PAMPs and DAMPs) results in greater cytokine secretion + inflammation
2
Q
how to treat severe covid
A
- immunotherapy: convalescent (recovering Pt) plasma transfusion
- neutrophils and macrophages are activated > swelling in lung tissue
- give IgA which is found in mucosa like covid > blocks and neutralises virus
3
Q
“long covid”
A
- health problems caused by COVID but have a later onset
4
Q
4 types of hypersensitivities
A
- type 1: immediate e.g. allergy, anaphylaxis (CANNOT have PAMPs or DAMPs)
- type 2: antibody mediated e.g. Graves disease
- type 3: immune complex mediated e.g. poststreptococcal glomerulonephritis
- type 4: T cell mediated e.g. T1D and RA
5
Q
2 types of cells involved in allergy
A
- mast cells: granules contain histamines, prostaglandins, heparin
- basophils: granules contain histamines and cytokines (IL-4 and IL-13)
- both IgE-mediated inflammation
6
Q
sensitisation (first step in allergy)
A
- allergen enters body and is phagocytosed (if skin > langerhans cell or if elsewhere, dendritic cells)
- presented to naïve Th cell on MHC II marker> TH2 cell secretes IL-4
- B cells differentiate into plasma cells > secrete IgE (class switching due to IL-4) which binds to mast cell and basophils from Fc region
7
Q
allergic response (second step)
A
- upon secondary exposure to allergen, allergen binds to IgE on mast cells > crosslinks
- leads to degranulation and release of histamine > allergic response
- 2 phases: immediate reaction phase using preformed chemical mediators (histamine) or late reaction phase using new chemical mediators (phospholipids, arachidonic acid, cytokines, prostaglandins)
8
Q
effects of histamine
A
- vasodilation
- leaky capillaries
- smooth muscle constriction
- oedema
9
Q
allergy immunotherapy
A
- allergen extract in tablet form
- administered sublingually
- takes years to develop immunity
- decreases mast cell and basophil activity and hence release of inflammatory mediators > prevent anaphylaxis
10
Q
what can immunotherapy be used for
A
- immunodeficiencies
- autoimmune diseases
- transplant rejections
11
Q
how do cancer cells evade detection
A
- stop expressing MHC I markers so CD8 (Tc) cells don’t recognise them
- express normal self antigens on MHC I so they blend in
- express ‘brake’ molecules that stop co-stimulation (signal 2) of T cells > anti-CTLA-4 or anti-PD-1
12
Q
‘brake’ molecules
A
- PD-1 binds to PD-L1 on T cell > T cell apoptosis > immunotherapy is anti-PD-1
- CTLA-4 binds to CD80/86 on APC > turns off T cells > immunotherapy is anti-CTLA-1
13
Q
3 types of immune control in a virus
A
- no control
- viral clearance
- viral persistance
14
Q
which cell doesn’t have PD-L1
A
- neutrophils
15
Q
the outcome of some viral infections can be transformation. what does this mean?
A
- virus has turned host cells into tumour cells
16
Q
monoclonal antibodies to treat systemic lupus erythematosus are specific for what?
A
BAFF