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Concepts of Disease > Immunology 3 > Flashcards

Immunology 3 Flashcards

1
Q

When does the innate immune system kick in?

A
  • If anatomical barrier, antimicrobrial proteins, peptides and phagocytes have all failed
  • Innate immune system will then induce inflammation
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2
Q

Name the five symtpoms of acute inflammation. (5 marks)

A
  1. Redness
  2. Heat (vasodilation and expanding of blood vessels)
  3. Swelling (causes the pain)
  4. Pain
  5. Loss of function
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3
Q

How does vasodilation contribute to inflammation? (3 marks)

A
  • 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
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4
Q

Explain what is happnening in this image of the ‘effects of cytokines released from activated phagocyte’. (4 marks)

A
  • 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
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5
Q

Explain what is happening in this image (5 marks)

A
  • 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
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6
Q

Name the different possible cells leukocytes could be. (4 marks)

A
  • Basophil
  • Neutrophil
  • Eosinophil
  • Monocyte
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7
Q

What happens during ‘leukocyte rolling’? (4 marks)

A
  • 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
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8
Q

What happens to the leukocyte specifically during ‘leukocyte rolling’? (6 marks)

A
  • 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
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9
Q

Give some of the chracteristics of a neutrophil e.g. location, cell type, mechanism

(4 marks)

A
  • 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)
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10
Q

How does the amount of neutrophils circulating increase in the blood stream?

(2 marks)

A

Infection → Bone marrow increases production of myeloid cells → signifcantly increases number of circulating neutrophils (leucocytosis)

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11
Q

How does NETosis occur by neutrohpils when killing a bacteria? (3 marks)

A
  • 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
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12
Q

What are the two different types of monocytes?

A

Classical: 90% - freely circulate and recruited to infection and become macrophages

Patrolling: roll along endothelial cell surface looking for injury

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13
Q

Can monocytes undergo repeated rounds of phagocytosis or just one?

A

Repeated

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14
Q

What triggers monocytes to migrate into the tissue?

A

In response to cytokines that macrophage has been released, and migrate to site of infection to undergo phagoyctosis

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15
Q

What is the lineage of mast cells and where are they found? (3 marks)

A
  • Myeloid lineage
  • Precursor mast cell in blood and they mature in tissue
  • Found in: skin, connective tissue, mucosal epithelial tissue, respiratory and digestive tract
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16
Q

What activates mast cells and what is the response that follows? (3 marks)

A
  • 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
17
Q

Which type of immune system are natural killer cells a part of?

A

Lymphoid lineage in the innate immune system

18
Q

How does a natural killer cell kill the pathogen after receiving the signal to?

(3 marks)

A
  • 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
19
Q

How does the natural killer cell distinguish between a healthy cell and an infected one? (5 marks)

A
  • 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
20
Q

Through which receptors dot B and T cells recognise their antigen?

A

TCR and BCR

(T/B cell receptor)

21
Q

What happens after a T cell differentiates into a CD8+ cell? (5 marks)

A
  • 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
22
Q

What happens when a t cell differentiates into a CD4+ cell? (4 marks)

A
  • 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
23
Q

What happens after a B cell is activated by a T cell? (3 marks)

A
  • 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
24
Q

How do dendritic cells trigger the adaptive immune system? (3 marks)

A
  • 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
25
Q

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

A
26
Q

Again - another question prob useful to look at table but cba to write out about 20 questions on it xoxoxo

A
27
Q

How does MHC I work as a antigen presenting molecule to ensure efficiency in the immune system? (4 marks)

A
  • 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
28
Q

How does a MHC II molecule work to ensure the immune system runs efficiently?

(4 marks)

A
  • 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)

29
Q

Why don’t erythrocytes present MHC I to show that they are a host cell?

A

They don’t have any DNA so no mahcinery for virus to work MHC II

30
Q

Why is the binding cleft of the peptide loose on a MHC I molecule?

A

So the molecule can ind to millionsof different peptide antigens

31
Q

How does MHC II presentation work on a molecular level? (3 marks)

A
  • 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
32
Q

How does MHC I present antigens on a molecular level?

(3 marks)

A
  • 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
33
Q

Learn the picture about MHC I molecules on the next slide

A
34
Q

Learn picture about MHC II molecules on next slide

A

Concepts of Disease (20 decks)

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