immunology Flashcards
(55 cards)
What is the difference between innate and acquired immunity?
- innate = rapid first response to infection
- no immunological memory
Acquired - lag time from exposure to response
(greater than 96 hours)
- immunological memory, responses are faster and more powerful, basis for protective vaccination against infectious disease
- specific for each antigen encountered
- self regulating through regulatory T cells
What are resident immune response cells (innate) and how do they recognise invading pathogens
- phagocytic (eating cells)- macrophages and dendritic cells
- others - mast cells
- pathogens - signature molecules (pathogens associated molecular patterns (PAMPS)
Innate immune cells - express partner receptors to these PAMPS called Pattern recognition receptors (PRRs)
Detail some modes of ingestion
- pinocytosis - ingestion of fluid surrounding cells
- receptor mediated endocytosis - molecules bound to membrane receptors are internalised
- Phagocytosis - intact particles (bacteria) are internalised whole which is facilitated by ‘opsonisation’
Draw a mental picture of the steps of phagocytosis
- macrophages express a set of PRRs
- Receptor binding to PAMPs signals the formation of a phagocytic cup
- cup extends around the target and pinches off, forming a phagosome
- fusion with lysosomes to form a phagolysosome - killing of pathogens and degradation of contents
- debris (antigens) is released into extracellular fluid
- pathogen-derived peptides are expressed on special cell surface receptors (MHC-2 molecules)
pro inflammatory mediators are released (TNF- alpha)
What is the definition of opsonisation?
coating of the pathogen by soluble factors (opsonins) to enhance phagocytosis
When are mast cells initiated? what is their mechanism?
- something that is too large to be engulfed invades (parasite)
- bind to the pathogen by PRR - PAMP - (degranulation - release of pre-formed pro-inflammatory substances (histamines))
- gene expression - production of new pro-inflammatory substances (leukotrienes and prostaglandins)
What leads to local, acute inflammation?
release of pro-inflammatory mediators - NO, prostaglandins histamines etc
How does inflammation affect healthy tissues?
- vascular changes
- recruitment and activation of neutrophils (transendothelial migration)
- chemicals are produced that attract neutrophils to the site of infection
What are the steps of transendothelial migration?
1 - margination of neutrophils to the endothelium near sites of damage
2 - binding of neutrophils to adhesion molecules on endothelial cells
3 - migration of neutrophils across endothelium via process of diapedesis
4 - movement of neutrophils within the tissues by chemotaxis
5 - activation of neutrophil by PAMPs and TNFalpha
What are the three jobs of neutrophils?
phagocytosis - use PRR to bind and phagocytose, killed using two mechanisms (phagolysosomal killing and Reactive oxygen species)
- degranulation - release of antibacterial proteins from neutrophil granules directly into extracellular environment can also cause tissue damage and systemic inflammation
- Neutrophil extracellular traps
How does reactive oxygen species work?
- NADPH oxygenase-dependant mechanism (repiratory burst) produces ROS
1 - neutrophil activation
2- assembly of the NADPH oxidase complex
3 - production and release of ROS into phagolysosome
How is the acute phase response driven?
- pro inflammatory mediators released by activated macrophages
- mediated by proteins secreted in the liver such as C3 and MBL (complement) and C reactive protein - primes bacteria for destruction by complement system)
How is a virus dealt with by the immune system?
- release cytokines called interferons which:
- signal neighbouring unaffected cells to destroy RNA and reduce protein synthesis
- signal neighbouring infected cells to undergo apoptosis
- activated immune cells such as natural killer cells - recognise and destroy virally-infected cells (and cancer cells)
What is the purpose of the complement system?
- opsonisation
- direct pathogen killing
- acute inflammation
- leukocyte recruitment§
Describe what the different pathways of the complement system to cleave C3?
Classical pathway, mannose binding lectin pathway and the alternative pathway
How does the mannose-binding lectin pathway work? - how does it lead to downstream complement pathway?
- MBL binds to manose on bacterium to activate C3 convertase to cleave into C3b and C3a - c3b turns into an alternative pathway to convert C3
- C3b then binds to pathogen surface and cleaves C5 into C5b and C5a - membrane attack complex is activated by C5b
- C3b is also involved in opsonisation
- C3a and C5a is used for acute inflammation
Why are dendritic cells so important?
bridge the gap between the innate immune response and acquired immune system responses
What are B and T cells involved in?
B cells - antibodies that attack pathogens circulating in the blood and lymph
key role in defence against extracellular pathogens
T cells - cellular immune response - defence against intracellular pathogens
CD4+ T cells - regulators of the entire immune system
CD8 T cells - kill infected body cells
How do B and T cells recognise pathogens?
pathogens have different antigens that are recognised by individual T and B cells
What type of cell is a B cell? what is its structure?
- it is an antibody
- complex of four polypeptide chains - 2 light chains and 2 heavy chains
- each antibody has a unique variable region that binds to 1 specific antigen
- can either be membrane bound or soluble
How does a T cell work?
- only recognise peptide antigens
- can express thousands of copies of a single antigen receptor
What condition must be filled in order for a T cell to recognise a peptide
can only recognise peptide antigens presented to their TCRs by MHC molecules
What is the function of Major histocompatibility complex?
display peptide antigens to T cells ( many different peptides to T cells)
What is the difference between class 1 and class 2?
class 1 - on nucleated cells, present peptide antigens to CD8+ T cells
class 2 - only on dendritic cells, macrophages and B cells
present peptide antigens to CD4+ T cells
