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LS10 C.elegans > Immunology > Flashcards

Immunology Flashcards

1
Q

Name 2/3 chemical/physical barriers

A

Lysozymes works as an antimicrobial agent

Defensins can kill bacteria or inhibit growth

Tight junctions can block the bacteria from entering

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2
Q

Name 3 outcomes of the complement system

A

Chemotaxis (recruitment of phagocytic cells)

Opsonization (phagocytes destroy the pathogen)

Lysis (formation of membrane attack complex which causes cell lysis)

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3
Q

What do phagocytes recognize?

A

PAMPS and ILCs

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4
Q

ILC-1 secretes….

A

IFNy which enhances macrophage function

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5
Q

ILC-3 secretes…

A

IL-17 and IL-22 to secrete chemokines and attract neutrophils

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6
Q

Name 4 phagocytes…

A

Macrophages, monocytes, neutrophils and dendritic cells

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7
Q

PAMPS/DAMPS =?

A

Pathogen associated molecular pattern/danger associated molecular pattern

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8
Q

PRRs function in…(3)

A

phagocytosis of microorganisms, cytokine production, and inducing co-stimulatory molecules in dendritic cells and macrophages

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9
Q

Name 4 ways of microorganism killing:

A

Degranulation of lysosomes, respiratory burts (ROS), NETosis (neutrophils), and nictric oxide pathway (macrophages, induced by IFNy, IL-1 or TNFa)

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10
Q

Why does the dendritic cells act as a bridge?

A

Once a dendritic cell recognizes a PAMP it will display the antigen and start T-cell activation

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11
Q

Name the 3 signals which are needed tor CD4+ T-cell activation

A
  1. MHCll/peptide binds to TCR
  2. Co-stimulation by CD80/86 binding to CD28
  3. Cytokine production by dendritic cells
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12
Q

Role of Th1…

A

Th1 stimulates macrophages as it secretes IFNy which enhances the nictric oxide pathway and allows CD40-CD40L binding (for B-cell activation!)

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13
Q

Role of Th17….

A

recruits neutrophils and IL-22 which induces anti-microbial peptides (only for extracellular bacteria!!)

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14
Q

Role of Tfh…

A

Helps the B-cell to produce IgG and allows opsonization of microbes

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15
Q

Name the 3 signals needed for B-cell activation

A
  1. whole antigen binding to BCR
  2. Co-stimulation by CD40-CD40L binding
  3. Secretion of cytokines (IL-21) and differentiation of the B-cell
    - -> into plasma cell
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16
Q

What’s thymus indepent antigen?

A

Can activate B-cells without Tfh, but does not make memory cells and there is no isotype switching so only IgM can be made

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17
Q

Name 5 functions of antibodies

A 
ADCC
Opsonization to enhance phagocytosis
Targeting complement pathway
Aggregation to clump bacteria together
Neutralization of bacterial toxins
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18
Q

Which type of IFN are produced by the presence of a virus?

A

IFN type 1, this produces IFNa and IFNb

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19
Q

How do NK cells recognize infected cells?

A

By absence of MHCl and the presence of PAMPS/DAMPS

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20
Q

How can a NK-cell kill?

A

Through TRIAL or via ADCC by IFNy and TNFa

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21
Q

Function of macrophages?

A

Macrophages can phagocytose and kill virus-infected cells, they secrete pro-inflammatory cytokines e.g. TNFa, nitric oxide and IFNa

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22
Q

Whats the difference between a naive and mature dendritic cell?

A

A naive dendritic cell can induce phagoycytosis but can not migrate
A mature dendritic cell can migrate and activate T-cell but can not induce phagocytosis

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23
Q

How is the antigen presented on MHCl? (nucleated cells)

A

The viral protein gets degraded by the proteasome and is transferred to the ER by TAP and is then loaded onto the surface by exocytosis

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24
Q

How is the antigen presented on MHCll (APCs)?

A

The viral protein gets phagocytoses and creates a phagosome, CLIP blocks MHCll and gets removed once HLA-DM opens MHCll up to enter the phagosome to get expressed on the surface through exocytosis

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25
Q

What is the function of cytotoxic T-cells?

A

They move to the site of infection and start killing the virus-infected cells

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26
Q

How do cytotoxic T-cells kill?

A

Through perforins and granzyme caspases which signal for apoptosis

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27
Q

Immunity =….

A

Recognition of non-self

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28
Q

Tolerance =…

A

Ignoring of self (tumors)

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29
Q

Central T-cell tolerance =…

A

It deletes T-cells with a high affinity to auto-antigens, this happens in the thymus

30
Q

Peripheral T-cell tolerance…

A

Regulates mature T-cells to avoid self-reactivity by anergy and Tregs, happens outside the thymus

31
Q

Where does T-cell development and activation take place?

A

In the bone marrow

32
Q

How does selection work in T-cells?

A

+ selection: T-cell recognize MHC in the cortex and advance to the medulla

  • selection: T-cells that recognize self-peptides in the medulla go through apoptosis, and the ones that don’t go into the circulation
33
Q

How are auto-antigens presented?

A

with AIRE which can present all possible self-antigens for it to become expressed by mTEC

34
Q

Whats the difference between natural and induced Treg?

A

Natural Treg are formed in the thymus and induced Treg are formed in the periphery from naive T-cells

35
Q

Name 4 functions of Tregs (how can they block the immune system?)

A

By blocking IL-2 production by Foxp3 of CD4+ T-cells –> T/B-cell die without IL2!
Expression of CD25 to capture IL-2
Expression of CTLA4, as it binds to CD80/CD86 to give off inhibition signals
Production of TGFb and IL-10 to induce regulatory/anti-inflammatory cytokines

36
Q

How does negative selection work in B-cell development?

A

If the B-cells bind to self-antigen they can either die or change their B-cell receptor and go through selection again (receptor editing)

37
Q

What do transitional B-cells do?

A

They express IgM and IgD to enter the periphery

38
Q

Auto-immunity=….

A

Loss of self-tolerance

39
Q

Auto-immune disease =….

A

The damage as a result of auto-immunity

40
Q

Systemic auto-immune disease =….

A

Auto-immunity on stuff that is present all over the body

41
Q

Why are mutations in AIRE, CTLA4, FOXP3, C1q, IL10RA/RB related to auto-immunity?

A

Because they are all produced by Treg, because Treg works to dampen the T-cell activation so there is more chance of an auto-immune disease

42
Q

Type 1 allergy mechanism…

A

IgE mediated, the allergen bind to IgE by recognition then the Fce receptor is bound to IgG and induces cross-linking which leads to mediator release e.g. hisamine

43
Q

Type IV allergy mechanism…

A

The antigen binds to the T-cell which releases cytokines that activate the macrophages which release the mediator, this is Th1 mediated

44
Q

Name 3 mediators

A

IL5+IL13 that amplify the Th2 response
IL6 + TNFa to promote inflammation and stimulate cytokine production
Histamine for extravastion, vasodilation and neuronal activation

45
Q

Name the 3 phases of immune surveillance…

A
  1. elimination, tumor growth rises in the tissue
  2. Equilibrium, pre-state of cancer
  3. Escape, the tumor cells escape from the immune sustem due to poorly immunogenic variants and subversion of the immune system
46
Q

Tumor antigen therapy =…

A

Injecting dead tumor cells and viable tumor cells to make antigen

47
Q

How can a tumor evade the immune system?

A

Not having enough PAMP so it will be treated as a self-antigen
Low immunogenecity
Tumors may mutate so it will not be recognzied anymore by the antigen

48
Q

Name 3 tumor-induced immune suppression…

A

TGFb and IL-10, they help induce Treg and attract it, so it will inhibit T-cells directly
Expression of PD-L1, this binds to the PD-L1 receptor on T-cells
Expression of IDO, which catabolizes tryptophan to kynurenine and inhibits the cell cycle arrest

49
Q

Name 5 methods to fight tumors

A 
Antibodies that recognize the tumor
Adoptive T-cell therapy by using T-cells from the tumor
Vaccines that provide immunogenecity
Nanoparticles
Checkpoint inhibitors
50
Q

Passive vaccines….

A

Vaccines with the addition of antibodies, fast and perfect for immunodeficient patients, but expensive and no memory cells are made

51
Q

Active vaccinations…

A

The antigen induces clonal expression of T/B-cells and form memory cells so that the next encounter is more rapid and effective

52
Q

Natural live vaccines…

A

You use a virus from another organism to make a vaccine

53
Q

Live attenuated vaccine….

A

You use a weakened pathogen that can not infect anymore, this can revert to its original type and become fatal

54
Q

Inactivated vaccines…

A

The antigen is inactivated by heat or formaldehyde, less effective then live vaccines but safer

55
Q

Vector vaccines…

A

You take a virus with a spike gene which can be active or inactive and you replicate it within the cells

56
Q

Recombinant vaccines…

A

Protein needs to made in yeast cells, to take up DNA and isolate it to achieve the protein

57
Q

Virus-like particles vaccine

A

You take an empty virus shell as a vaccine to mimic the structure of the virus, so not infectious as they lack genetic material

58
Q

DNA/RNA viruses

A

In DNA you create pores in the membrane so that it can uptake DNA into the cell, for RNA you encase it in a lipid coat so that it can enter the cell te become replicated and make genetic material for it to cause an immune response

59
Q

Toxoid vaccines…

A

The toxin is produced and inactived through heat or formaldehyde to start an immune response to get toxin-specific antibodies

60
Q

Conjugate vaccines…

A

Combining T-independent sugar with a protein so it can present the protein part and still recognize the sugar part inside (the T-cell independent part)

61
Q

Whats the disadvantage of mucosal administration?

A

The antigen can degrade and induce tolerance to the antigen

62
Q

Why are adjuvants used?

A

To enhance the immune response, so you can use fewer does, get a faster immune response and to get long-lasting immunity

63
Q

Name 5 immunostimulants…

A

Alum, binds to the antigen/PRR so that dendritic cells can mature and stimulate inflammation
Mineral oils that bind to TLRs
PAMPs
Depot formation, to cluster antigens and PAMPS together

64
Q

Whats the difference between primary and secondary immunodeficiencies?

A

Primary are genetical and heritable, here you have intrinsic defects in the cells of the immune system
Secondary are acquired during life by e.g. malnutrition, trauma, HIV, chemo etc.

65
Q

Whats the difference between specific and non-specific immunodeficiency?

A 
Specific = T/B-cells
Non-specific = Complement system and phagocytes
66
Q

X-linked agammaglobulinemia (X-LA)…

A

there are no antibodies because the BCR doesnt function so they never leave the bone marrow, you can have T-cells but no memory cells can be made

67
Q

Hyper-IgM, CD40-CD40L deficiency…

A

B-cells can only produce IgM because isotype switching can not take place –> no B-cell activation

68
Q

SCID…

A

no thymus development so no invasion of the thymus by lymphoid cells because of a defective y-chain of IL-2 receptor or RAG1/2 deficiency

69
Q

MHCll deficiency…

A

APCs do not have MHCll so there are no CD4+ T-cells present as there is no selection, so also no CD8+ T-cells, no Treg and only IgM can be made

70
Q

Phagocytic deficiency…

A

Here you have defective NADPH oxidase so bacteria wil stay alive inside the phagocytes as there is no respiratory burst

71
Q

LAD1/2 deficiency…

A

problems with migration so the cells do not stop at the site of infection and requires a lot of energy
LAD-1: problem with adhesion
LAD-2: Siayl Lewisx binds to L-selectin so there is a problem with rolling

72
Q

HIV…

A

The CD4+ T-helper lymphocytes are depleted which weakens the immune system so the body can not stop infections or remove cancer cells

LS10 C.elegans (4 decks)

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