Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What do phagocytes recognize?

A

PAMPS and ILCs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

ILC-1 secretes….

A

IFNy which enhances macrophage function

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

ILC-3 secretes…

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Name 4 phagocytes…

A

Macrophages, monocytes, neutrophils and dendritic cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

PAMPS/DAMPS =?

A

Pathogen associated molecular pattern/danger associated molecular pattern

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

PRRs function in…(3)

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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!)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Role of Th17….

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Role of Tfh…

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

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

A

IFN type 1, this produces IFNa and IFNb

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

How do NK cells recognize infected cells?

A

By absence of MHCl and the presence of PAMPS/DAMPS

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

How can a NK-cell kill?

A

Through TRIAL or via ADCC by IFNy and TNFa

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

How do cytotoxic T-cells kill?

A

Through perforins and granzyme caspases which signal for apoptosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

Immunity =….

A

Recognition of non-self

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

Tolerance =…

A

Ignoring of self (tumors)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2025 Bold Learning Solutions. Terms and Conditions