Immunology Flashcards
T/ B cell involved in innate immunity
IgM antibody production by CD 5+ subset of B cells
Main signalling molecules in bacterial damage and phagocytes recruitment
Cytokines
TNF - alpha
IL-1
Chemokines/ IL-8
3 complement pathways
Classic
Alternate
Mannose binding lectin
3 main purposes of complement
- label micro-organisms ( i.e. opsonisation)
- recruit phagocytes (i.e. chemotaxis)
- destroy- microorganisms by perforating the cell membrane (i.e. cytolysis)
How many main protein in complement cascade
9 complement proteins
Protein of MAC
C5-8 which then activate lots of C9s in a ring to form the MAC
Inflammatory complement mediators
C3a - the best,
C5a - pretty good,
C4 - pretty useless
Trigger(s) for classic complement pathway
IgG antibody (bound to something)
- therefore needs the adaptive immune system to have already worked
Other triggers
* Aggregated immunoglobulin
- Some RNA viruses
- Staphlococcal protein A
- Polyanions and cations e.g. heparin
- C-reactive protein
- Some proteolytic enzymes
Trigger(s) for alternate complement pathway
Main:
- C3 binding to bacteria
Other
* Aggregated immunoglobulins
* C3 nephritic factor (antibody to an enzyme activating C3)
- LPS (endotoxin)
- Some acute phase proteins i.e. mannose binding protein, C reactive protein
- Radiographic contrast media
- Plant and bacterial polysaccharides
Is the membrane attack complex (MAC) better in gram neg or pos bacteria
much more effective in gram negative
Mechanisms for protection of host cells against complement (MAC)
Membrane-bound complement inhibitors on cells include:
- DAF (decay accelerating factor) and MCP (membrane cofactor protein) which break down C3 convertase
- HRF (homologous restriction factor) C8 binding protein and CD59 which prevent the formation of MAC on host cells
DAF, MCP
Decay accelerating factor
Membrane cofactor protein
break down C3 convertase
HRF
homologous restriction factor
- C8 binding protein and CD59 which prevent the formation of MAC on host cells
Alternate name NK cells
large granular lymphocytes
NK cells and MHC class signalling
inhibited when they recognise their own MHC Class I molecules on target cells
kill target cells in which MHC Class I molecule expression has been down-regulated allowing escape from CTLs
also recognise other activating (and inhibiting) receptors on the surface of target cells
NK cells and antibodies
NK cells can acquire antibody (Fc portion of IgG) via CD16 Fc receptors allowing specific antigen recognition - ADCC
THings released by NK cells
perforins and granzymes to kill cells
Make interferon gamma
NK cells and MHC 2
no relation/ no interaction
Main cytokine that increases body’s temp/ set point
IL-1
Cytokines from macrophages that increase selectin and integrins activation on endothelial cells
TNF-alpha
Il-1
Cytokine that causes liver to release inflamamtory things
TNF-alpha
IL-1β and IFN-γ and IL-6 also very improtant
Cytokines released by DCs after activation by TLRs?
IFN-alpha/ beta
TNF-alpha
IL-6
IL-12
Increased surface expresison molecules in DC after activation
CD 80.86
MHC - II
CD 40
HLA molecules encoded by genes on which chromosome
6