lecture 11

Question 1

what is the difference between the immune response of animals and plants?

Answer 1

in animals, recognition of a microbial invader is usually followed by engulfment by a phagocytic cell. plants lack this response

Question 2

what are the three major classes of phagocytes?

Answer 2

neutrophil , it’s the most abundant
eosinophil , it works in groups
macrophage , it is very large in size

neutrophils and eosinophils are granulocytes, because their cytoplasm is granular
microphages are from an agranulocyte lineage but as they mature they develop granules
they contain numerous lysosomes and secretory vesicles

Question 3

formation of macrophages

Answer 3

monocytes mature to become macrophages

most cells can also go through phagocytosis, but the three major classes of phagocytes on major dedicated phagocytes

Question 4

describe neutrophils

Answer 4

they are the most common type of granulocytes and they are also called polymorphonuclear leukocytes because of their multi lobed nucleus

they phagocytose and destroy microorganisms like bacteria (so they are important in the innate immunity to bacterial infection)

they’re short-lived cells
abundant in blood
not present in normal healthy tissues

Question 5

neutrophils are rapidly recruited to site of infection by

Answer 5

rapidly recruited by
activated macrophages peptide
fragments of cleaved complement proteins
PAMPs

neutrophils respond to cries of macrophages
they are very sensitive to cleaved complement proteins

Question 6

describe macrophages

Answer 6

they are much larger and longer lives than neutrophils
they recognise and remove senescent dead and damaged cells in many tissues
they’re able to ingest large microorganisms such as protozoa

Question 7

describe eosinophils

Answer 7

they help to destroy parasites and also modulate allergic inflammatory responses

if a bacteria is too large then it needs to be coated with compliments for the eosinophils to recognise and collectively kill it

they destroy the parasites in us and have an effect on certain allergic responses

Question 8

how do phagocytes engulf their targets

Answer 8

phagocytes display cell surface receptors for pamps and chemicals produced by the immune response:

• TLRs
• receptors for antibodies produced by the adaptive immune system
• receptors for complement c3b protein

the binding of ligands to any of these receptors activates phagocytes which enhances the killing power and causes the release of cytokines to attract more white blood cells
it also induces actin polymerization at the site:
the phagocyte’s plasma membrane surrounds the pathogen in an attempt to in golf fit in a large membrane enclosed phagosome

Question 9

define the granules found in granulocytes

Answer 9

the granules are dense membrane-bound lysosomal derivatives
they fuse with the phagosome membrane and release their contents in an attempt to digest the pathogen cell wall
this activation activates an army and the granules are lysosomal and they migrate towards the site of actin polymerization to fuse with phagolysosome and empty lysozyme enzymes into it

Question 10

what are NADPH oxidase complexes?

Answer 10

they form on the phago-lysosomal membrane
a respiratory burst by the facts site allows the NADPH oxidase complexes to produce highly toxic oxygen derived compounds

this is called the respiratory burst where they convert the oxygen into a superoxide which is extremely damaging or into hydrogen peroxide which is bleach

Question 11

which phagocytes survives this chemical and enzymatic barrage?

Answer 11

most macrophages survive it but neutrophils do not

neutrophils appear to be suicide squads and will even use their own DNA to accomplish their task by ejecting it in a sticky web that can trap bacteria preventing the escape from the killing Frenzy

passes made out of dead neutrophils and pathogens, and it is sticky because of the DNA that is exposed

Question 12

how can pathogens survive this killing frenzy?

Answer 12

the addition of silac acid to capsule components avoids complement attack and subsequent engulfment

some bacteria survive and replicate inside the neutrophils by expressing virulence factors that protect against the respiratory burst until the neutrophil die

some bacteria can neutralise actin polymerization and phagocytosis by injecting a toxin that disrupts the actin cytoskeleton assembly

some bacteria can survive inside macrophages and can use the macrophage as it migrates away. this converts a local invasion into a severe systemic disease

Question 13

how does inflammation aid the killing frenzy?

Answer 13

symptoms of inflammation have been recognised for a long time medically
blood vessels dilate leading to local swelling and the accumulation of components of the complement cascade

activation of tlrs in epithelia and activated macrophages contribute to inflammation (macrophages also secrete cytokines like chemokines that attract neutrophils)

Question 14

symptoms of inflammation

Answer 14

dolor as pain
rubor as redness
calor as heat
turgor as swelling

Question 15

extreme cases of inflammation

Answer 15

systemic release of inflammatory cytokines can lead to excessive blood vessel dilation, resulting in sudden lowering of blood pressure
if widespread inflammation, swelling and blood clotting occurs –> this is septic shock

the sudden decrease in blood pressure can reduce blood supply to vital organs

Question 16

how are virus-infected cells dealt with by innate immunity?

Answer 16

viruses invade cells, and host cell ribosomes make viral proteins
host cell lipids are used in the construction of new enveloped viruses
there is not much opportunity for the cell to display virus encoded pamps at the self-service

the innate immune system generally relies on:

• recognition of CPG motifs in viral DNA by tlr9 (TLR are usually found on the plasma membrane but some are active on internal membranes where they aid in detecting internal pathogens)
• recognition of viral dsRNA that is an intermediate in the lifecycle of many viruses

Question 17

how does dsRNA induce interferon IFN production?

Answer 17

once a cell is infected the dsrna can induce interferon production which will induce changes in the cell itself by autocrine action
it can also induce changes in neighbouring cells by paracrine action

interferons are cytokrines that interfere with viral infection and they are the most important cytokines in the virology context

Question 18

how do IFNs limit viral replication and spread?

Answer 18

1. they make the virally infected cell and its neighbouring cells into much less efficient factories for making viruses
   (communication between cells is increased, deactivate a ssrna nucleus which degrades host ssrna which reduces host protein synthesis, and they activate mechanisms that down host cells synthesis in neighbouring cells)
2. they limit viral spread by promoting apoptosis of the infected cell
3. upregulate the display of viral peptides on the outer membrane of the infected cell to provide signals for recognition by activated t cells
4. they stimulate expression of the immunoproteasome to process and destroy viral proteins (immunoproteasome is a protein destructive complex with a barrel of 4 rings and the targeted protein enters the centre, is destroyed in the middle and exits as peptides)
5. they also provide a call for help to attract natural killer cells and to activate macrophages
6. they also fight cancers

Question 19

define the natural killer cells and how they work

Answer 19

many viruses and cancers downregulate the expression of immune system recognition molecules on the cell surfaces. this cell will likely be infected or transformed.

natural killer cells recognise their targets by monitoring the level of expression of these molecules at the cell surface. they also are attracted to virally infected cells by IFNs.
natural killer cells then persuade such cells to commit suicide which is apoptosis

Question 20

how do natural killer cells persuade their targets to apoptose?

Answer 20

apoptotic signals are sent
mild convolution, chromatin compaction, cytoplasmic condensation
nuclear fragmentation, cell blabbing, cell fragmentation
phagocytosis

this is the same method used by cytotoxic t cells