9 Host Defence Overview Flashcards
Q: What is the role of the immune system? (2)
A: defend against viruses, bacteria, fungi and parasites
has to detect and react to dangerous ones (differentiate from the foreign but safe)
Q: Name 2 ideal modes of transmission. Compare.
A: respiratory infections that spread via sneezes- droplet etc
upper GI tract- when vomiting
-> less effective as it’s easier to avoid
Q: When do you experience most colds in you life?
A: 1st year of life
Q: Describe how evolution of flu viruses works against us.
A: if we are infected by one strain and our immune system is competent we gave immunity to it
but if virus keeps evolving so that our antibodies/humeral response don’t match -> we can keep getting infected
Q: What are the mechanical defences? (3)
A: -epithelial tight junctions (integrity)
- skin waterproofed by fatty secretions
- social conditioning eg washing hand
Q: What are the chemical defences? (5)
A: -fatty acids (on skin) have antimicrobial properties
- enzyme lysozyme in saliva, sweat and tears
- enzyme pepsin in gut
- low pH in stomach and sweat
- antimicrobial peptides in paneth cells in intetine
Q: What are the microbiological defences? (2)
A: -normal flora compete for nutrients/attachment sites
-production of antimicrobial substances
Q: What is the first and the last barrier concept?
A: skin surface is made of dead or dying cells
even if they get infected they will slough off or die so disease does not spread
Q: What are the surface defences against infection? (7)
A: -Coughing -Sneezing -Mucus -Cilia => mucocillary escalator which takes things to back of throat to be swallowed to enter low pH of stomach -Rapid cell turnover -Wall of dead cells
Q: Describe one way smoking promotes infection.
A: weakens action of cilia/confuses them
Q: What do type I mucosa cells line? (4) Structure? (2)
A: gut, ciliated respiratory, upper vagina, posterior nose
=>includes cilia, single layer
Q: What do type II mucosa cells line? (5) Structure? (2)
A: cornea, mouth, oesophagus, lower vagina, anterior nose
=> flat, multi layered
Q: Describe the sequential action of the immune system. (3) How do they vary? (3)
A: events occur in specific order
pre-infection/ ‘first line’
early infection/ ‘second line’
late infection/ ‘specific/acquired’
- specificity increases
- breadth decreases
- learning increases
Q: What is involved in preinfection? (3)
A: -avoidance
- mucus
- physical barriers
Q: What is involved in early infection? (6)
A: -phagocytes
- opsonins
- some lymphocytes
- interferons
- acute phase proteins
- toll-like receptors
Q: What is involved in late infection? (2)
A: -T cells
-antibody
Q: What’s involved in innate sensing? (3)
A: detecting PAMPs and DAMPs and differentiating between what’s dangerous and what’s not
Q: What are PAMPs?
A: Pathogen-associated molecular patterns are molecules associated with groups of pathogens, that are recognised by cells of the innate immune system
Q: What are DAMPs?
A: danger-associated molecular patterns, danger signals, and alarmin, are host biomolecules that can initiate and perpetuate a noninfectious inflammatory
host biomolecules that can initiate and perpetuate a noninfectious inflammatory response.response
Q: What happens when PAMPs and DAMPs are recognised? Difference?
A: the cells produce interferons and a wave of information spreads out
danger-associated molecular patterns initiate and perpetuate a NONinfectious inflammatory response
pathogen-associated molecular patterns (PAMPs) initiate and perpetuate the INFECTIOUS pathogen-induced inflammatory response.
Q: What are the types of interferons? (3) When are they activated? What do they do? (5,2)
A: Type I/III: alpha/beta/lamda => important in early stage of infection -activation of neighbouring cells -Activates NK cells -Upregulates MHC and Mx proteins -Activates RNase L and Protein Kinase R (PKR) -Induces anti-viral state
Type II: IFNgamma (interferon gamma)
- Proinflammatory
- Th1 cytokine
Q: What releases type I/III interferons? II?
A: all nucleated cells in response to infection
T cells
Q: Summarise the role of phagocytes. What happens within?
A: engulf invaders-> antigen is destroyed in intracellular vesicles
Q: What’s the importance of IgA?
A: defence on mucosal surface
Q: What is the basic structure of antibodies? (2)
A: Fab: antigen binding part = variable
Fc= binds to host sensors
Q: What are the possible actions of antibodies? (3)
A: -direct neutralisation (prevents binding and entering cells)
- opsonised and engulfed
- agglutination
Q: What does each T cell express? What does this see?
A: one TcR
-each TcR sees a specific combination of MHC and peptide at high affinity
Q: What are the 2 types of T cells? Role? (1,3)
A: cytotixic (CTL)- kill target cells
helper T- activate macrophages to kill, B cells to secrete antibodies and CTL to kill
Q: Name 6 defences against viruses. Most important? Name 6 defences against bacteria.
A: 1. Surface defences
- Inflammatory mediators and acute phase proteins
- Antibody, complement, ADCC (antibody dependent cell-mediated cytotoxicity)
- NK cells
- T cells (mostly resolving infection)
- Interferons - VERY IMPORTANT AGAINST VIRUSES - Surface defences (mechanical and chemical)
- Release of inflammatory mediators and acute phase proteins (and opsonins)
- Antibody opsonisation
- Complement (alternative pathway) causing lysis/opsonisation
- Phagocytosis
- Fever
Q: What is a cytokine storm? Can lead to? (5)
A: a dis-regulated exaggeration production of pro-inflammatory cytokines
leads to excessive accumulation of inflammatory cells, pulmonary oedema and eventually lung damage and airway occlusion potentially resulting in death
Q: What are the characteristics of an eradicable infectious disease? (5)
A: -simple (and cheap) to diagnose
- genetically stable pathogen
- accessible host species
- eliminates persistent infection OR persistently infected host can’t transmit
- safe and effective vaccine
