Immunology 3 Flashcards
When does the innate immune system kick in?
- If anatomical barrier, antimicrobrial proteins, peptides and phagocytes have all failed
- Innate immune system will then induce inflammation
Name the five symtpoms of acute inflammation. (5 marks)
- Redness
- Heat (vasodilation and expanding of blood vessels)
- Swelling (causes the pain)
- Pain
- Loss of function
How does vasodilation contribute to inflammation? (3 marks)
- Causes endothelial contraction of endothelial cells on lumen of blood vessels - thus inducing plasma leakage
- As gaps between endothelial cells increase, plasma leaks out more of the capillaries thus increasing fluid, swelling and pain
- Nociceptors pick up on increase in pressure and send pain signals to rest of tissue
- Damage broken blood vessels have blood leakafe inot tissue causing a kinin respone and bradykinin binds to nociceptors and increases the pain signal
Explain what is happnening in this image of the ‘effects of cytokines released from activated phagocyte’. (4 marks)
- endothelial cells lining capillary have leukocyte readily avaible flowing in middle of blood vessel
- Phagocytic cell thats encountered pathogen is activated
- Cytokines reach endothelial cells outside of capillary driving many of processes for inflammation
Explain what is happening in this image (5 marks)
- the cytokines instruct smooth muscles cells in arteriole to undergo vasodilation and expand volume in arteriole which will slow down flow
- Leukocytes tumbel along as flow of blood is slower
- Have increased gaps between endothelial cells when cytokines bind
- Less damage to blood vessels only plasma comes out and increases amount of proteins in that area
- cytokines induce expression of adhesion molecules on luminal sie of endothelial cells and increase in cell adhesion molecules will grab hold of leukocytes
Name the different possible cells leukocytes could be. (4 marks)
- Basophil
- Neutrophil
- Eosinophil
- Monocyte
What happens during ‘leukocyte rolling’? (4 marks)
-
Cell adhesion molecules are expressed by endothelial cells
- (because cytokines have induced expression)
- Cell adhesion molecules grab hold of leukocytes by slings covered in oligosaccharides
- Endothelial cell grabs hold of these and slows movement of leukocyte even more
- Leukocyte is continulally attached to endothelial cells but it’s just rolling along
What happens to the leukocyte specifically during ‘leukocyte rolling’? (6 marks)
- leukocyte expresses integrin and enthothelial cell secretes IL-8 in response to cytokines
- IL-8 binds to leukocyte IL-8R on rolling leukocyte and increases affinity of integrin for ICAM
- Endothelial cells are expressing two molecules: one that grabs a sling and the other being ICAM
- Intefrin binds to ICAM - consequently bringing leukocyte to a halt
- leukocyte is directed through endothelial layer by other cell adhesion molecules
- leukocyte attracted to site of infection by attractants released by phagocyte
Give some of the chracteristics of a neutrophil e.g. location, cell type, mechanism
(4 marks)
- Major WBC/ circulating leukocyte
- Not found in healthy tissue
- contains granules that have defensins and cathelicidins (granulocyte)
- Mechanisms of killing pathogens:derganulation, NETosis (NET- neutrophil extracellualr traps)
How does the amount of neutrophils circulating increase in the blood stream?
(2 marks)
Infection → Bone marrow increases production of myeloid cells → signifcantly increases number of circulating neutrophils (leucocytosis)
How does NETosis occur by neutrohpils when killing a bacteria? (3 marks)
- After phagocytosis some neutrohpils don’t apoptose and throw out their chromatin from cell to create a trap
- After neutrophil dies, it has thrown out its DNA and caught any bacteria in local vicinty so it can’t go on to infect other cells
- but phagocytes can kill them
What are the two different types of monocytes?
Classical: 90% - freely circulate and recruited to infection and become macrophages
Patrolling: roll along endothelial cell surface looking for injury
Can monocytes undergo repeated rounds of phagocytosis or just one?
Repeated
What triggers monocytes to migrate into the tissue?
In response to cytokines that macrophage has been released, and migrate to site of infection to undergo phagoyctosis
What is the lineage of mast cells and where are they found? (3 marks)
- Myeloid lineage
- Precursor mast cell in blood and they mature in tissue
- Found in: skin, connective tissue, mucosal epithelial tissue, respiratory and digestive tract
What activates mast cells and what is the response that follows? (3 marks)
- Activated by complement proteins - which bind to mast cells and induce inflammation by inducing degranulation
- Degranulation = granules being thrown out of mast cell which induces vasodilation and itching and airway constriction IF it goes wrong
- Heavily involved in allergy reponses
Which type of immune system are natural killer cells a part of?
Lymphoid lineage in the innate immune system
How does a natural killer cell kill the pathogen after receiving the signal to?
(3 marks)
- Forms a synapse between NK membane and target cell
- Releases perforin which creates pores in cell by polymerisation
- NK cell releases granzyme which induces apoptosis and persuades target cell to kill itself as it activates the apoptotic pathway
How does the natural killer cell distinguish between a healthy cell and an infected one? (5 marks)
- Healthy cell display activating and inhibitory signals on its cell surface
- Inhibitory signals present the cell peptide to show its a healthy cell and therefore inhibiting the natural killer cell from killing it
- A malignant cell will show the healthy host protein but will present more signlas that are unhealthy showing it is bad
- Signals will cause the balance to tip and this will kill it
- Reduction in self inhibitory signal and increase in activating signal causes NK to induce apoptosis
Through which receptors dot B and T cells recognise their antigen?
TCR and BCR
(T/B cell receptor)
What happens after a T cell differentiates into a CD8+ cell? (5 marks)
- Pathogen infect inside of cell and will present parts of its virus on cell using MHC I molecules
- T cell recognises this and is activated
- T cell becomes cytotoxic
- Clonal expansion
- Cells infected and display that they are infected with MHC molecules
- Interaction is very specific
What happens when a t cell differentiates into a CD4+ cell? (4 marks)
- specifcally recognise a broken bit of pathogen
- MHC II is presenting pathogen for CD4+
- T cell activated and becomes t helper cell and gets involved with b cells
- T helper cell interact with humoral part of immune system by activating b cell
What happens after a B cell is activated by a T cell? (3 marks)
- B cell phagocytose bacteria - which is recognised by T cell
- B cell now activated and either become memory cell or plasma cell and release lots of antibodies
- Plasma cells clone and are able to recognise a particular pathogen
How do dendritic cells trigger the adaptive immune system? (3 marks)
- Immature dendritic cells reside in peripheral tissues
- Dendritic cells migrate via lymphatic vessels to regional lymph nodes
- Mature dendritic cells activate naive T cells in lymphnoid organs i.e. lymph nodes
This is here so that you can REPEATEDLY (score 1/2 for basically every time) look at teh locations of the adaptive cells - probably useful
Again - another question prob useful to look at table but cba to write out about 20 questions on it xoxoxo
How does MHC I work as a antigen presenting molecule to ensure efficiency in the immune system? (4 marks)
- Prevents proteins being degraded into peptides on self cells
- Presents peptides frombroken down intracellular infection
- Regulates killer cell activity - MHC I either present host cell or pathogen antigens
- Presentation of pathgoen antigen activates CD8+ T cell - becomes cytotoxic and kills cell, inducing apoptosis
How does a MHC II molecule work to ensure the immune system runs efficiently?
(4 marks)
- Present antigens from pathogen that has been phagocytosed - either macrophage or dendritic cell
- Phagocytosed pathogen antigens presented on MHC II surface
- Above process causes activation of CD4+ T cells which recognise it and cause a cascade of activating B cells with produce antibodies
(antigen presenting cells in particular use MHC II)
Why don’t erythrocytes present MHC I to show that they are a host cell?
They don’t have any DNA so no mahcinery for virus to work MHC II
Why is the binding cleft of the peptide loose on a MHC I molecule?
So the molecule can ind to millionsof different peptide antigens
How does MHC II presentation work on a molecular level? (3 marks)
- Pathogen phagocytosed and in phagolysosome being destroyed
- MHC II translated in ER and processed in Golgi and released into endosome where it travels to phagolysosome to meet the broken down peptides of the pahgocytosed pathogen
- Pathogen then transported to surface where it is presented
How does MHC I present antigens on a molecular level?
(3 marks)
- Presents antigens from host cells
- Proteosome breaks down proteins and turns them into short peptides which are transported to the ER
- MHC I comes across peptide in ER and picks it up there and transports it to the surface
Learn the picture about MHC I molecules on the next slide
Learn picture about MHC II molecules on next slide
