immunology 2 Flashcards
describe the steps in the complement system
- C3 is cleaved into the active C3a and C3b
- C3b can then cleave C5 into C5a and C5b
- C3b can then amplify the reaction via the alternative pathway, causing more C3 to cleave into C3a and C3b
- C5b (along with other factors) produces the membrane attack complex, which inserts into cell walls and destroys the cell by letting salt and water in
- C3a and C5a are responsible for acute inflammation (they are anaphylatoxins)
explain how Macrophages work
- Macrophage expresses PRR’s.
- Receptor binding to PAMP’s signals formation of phagocytotic cup.
- Cup engulfs the target forming a phagosome.
- Phagosome fuses with lysosome, forming a phagolysosome.
- Debris are released into extracellular fluid. MHC-II molecules and TNFa are released
(facilitated by opsonisation)
explain opsonisation
the coating of pathogens by soluble factors (opsonins) to enhance phagocytosis
- C3b
- IgG/IgM
- CRP (c reactive protein)
explain how Mast cells work
- they deal with pathogens too large for phagocytosis
- PRRs on mast cell bind to PAMPs on pathogen, the mast cell is stimulated to release pro-inflammatory substances such as HISTAMINE and TRYPTASE
- As this happens, the mast cell also beings to produce more pro-inflammatory substances (histamine, TNF, chemokines)
explain transendothelial migration
- the recruitment of neutrophils to the site of infection/damage during acute inflammation
- Margination of neutrophils to site of damage. Neutrophils bind to adhesion molecules.
- Neutrophils migrate across endothelium (diapedesis)
- Neutrophils move within tissues.
- Activation of neutrophils by PAMP’s and TNF⍺
explain the killing mechanisms of neutrophils
NETs: release a net-like structure that traps pathogens, leading to phagocytosis.
Phagocytosis: pathogens release chemical signals that attract neutrophils, which use PRR to bind to and phagocytose these pathogens.
Degranulation: anti-bacterial proteins released from neutrophil granules directly into the extracellular matrix
(CAN DAMAGE SURROUNDING TISSUES)
what are the types of endocytosis?
Pinocytosis: ingestion of fluid from surrounding cells
Phagocytosis: bacterium engulfed by cell surface
Receptor mediated endocytosis - molecules bound to membrane receptors are internalised
(important in the generation of adaptive immunity)
describe B cell activation
- Membrane-bound antibodies on the B cells bind to target antigen IgM within the B cell zone of lymph nodes
- B cells require 2 signals to become fully active and begin proliferation - the antigen and helper signals
- Helping signals→ Non protein antigens = PAMPS and PRR. Protein antigens = Tfhcells
- Once activated, they clonally proliferate and become either a plasma cell (antibodies) or a memory B cell - germinal centre response
- High affinity antibodies are generated→ IgM (produced by plasma cells)→ IgG (produced by B cells responding to certain antigens), assisted by TH cells
- The final response B cells have in the immune system is they differentiate into long lived memory B cells
describe the transport of lymphocytes
Lymph and lymphocytes leave lymph node → medullary sinus → efferent lymphatic vessels → blood circulation via lymphatic ducts at the subclavian vein
what is the job of CD4+ (helper) T cells
activate B cells & stimulate production of memory B cells
what is the job of CD8+ (killer) T cells
kill infected cells via perforin/granzymes/granulysin
Describe T cell activation
→T cells can only recognise peptide antigens
- Dendritic cells recognise and phagocytose antigenic debris
- In the presence of pro-inflammatory mediators (e.g. TNF⍺), the dendritic cells mature and increase expression of stimulatory molecules on their surface
- Dendritic cells phagocytose the pathogenic antigens, break the antigens down into short peptides and load them onto MHC II molecules
- MHC II molecules transported to cell surface
a) At the same time, the maturing dendritic cells migrate into the lymph nodes via the afferent lymphatic vessels - Co-stimulatory molecules enable T cell to respond to antigen and fully differentiate
