Immunology Test 1

Front 1

What generate TCR Binding Diversity?

Back 1

1. Rearrangement of the β chain VDJ segments.
2. Rearrangment of the α chain VJ segments
3) Junctional diversity between gene segments

Front 2

What's SCID disease?

Back 2

T and B cells fail to rearrange their TCR and Ig genes,

Front 3

What are two subsets of T cells?

Back 3

CD4 and CD8

Front 4

CD4T cell recognizes what kind of pathogen?

Back 4

Extracellular pathogen presented on MHC II.

Front 5

CD8T cell recognizes what kind of pathogen?

Back 5

Intracellular pathogen presented on MHC I.

Front 6

Structure of CD4 co-receptor.

Back 6

1 transmembrane chain. (D1-D4)

Front 7

Structure of CD8 co-receptor.

Back 7

2 transmembrane chains. (alpha and beta)

Front 8

Structure of MHC Class I.

Back 8

- 1 heavy alpha chain.
- beta microglobulin
- Peptide size range from 8-12 amino acids.

Front 9

Structure of MHC Class II.

Back 9

- 2 chains (alpha and beta)
- 12-25 amino acids in length.
- Presented on APC (B cells, DC, macrophages)

Front 10

Preferred amino acid position on HLA-A MHC Class I.

Back 10

2, 6, 9. (HIV Reverse Transcriptase)

Front 11

Preferred amino acid position on HLA-B MHC Class I.

Back 11

2, 9 (Measles Virus F proteins)

Front 12

Preferred amino acid position on HLA-DRB MHC Class II.

Back 12

1, 4, 9

Front 13

CD8 binds to what domain of MHC I?

Back 13

alpha3 domain

Front 14

CD4 binds to what domain of MHC II?

Back 14

beta2 domain

Front 15

Peptides degraded in cytosol bind to what MHC molecule?

Back 15

MHC Class I

Front 16

Peptides degraded in endocytic vesicles bind to what MHC molecule?

Back 16

MCH Class II

Front 17

MHC Class I molecule is presented on what cells?

Back 17

T cells, B cells, Macrophages, DC, Neutrophils

Front 18

MHC Class II molecule is presented on what cells?

Back 18

B cells, macrophages, DC

Front 19

What is MHC restriction?

Back 19

Antigen specific T cell response is restricted by MHC type.

For example:
- CD8T cell specific for peptide X with MHC Class I HLA-A.
- TCR doesn’t recognize the same peptide when it’s bound to MHC Class I HLA-B.
- TCR doesn’t recognize a different peptide Y with MHC Class I HLA-A.

Front 20

How many binding sites does a TCR have?

Back 20

1

Front 21

How many binding sites does an Ig have?

Back 21

At least 2.

Front 22

T/F. TCR changes it affinity on encountering antigen.

Back 22

False.

Front 23

T/F. TCR doesn't isotype switch.

Back 23

True.

Front 24

T/F. Somatic hypermutation occurs in TCR.

Back 24

False.

Front 25

T/F. TCR's are used to recognize antigens only.

Back 25

True.

Front 26

What are the functions of AID enzyme?

Back 26

Helps B cell:
1. Somatic Hypermutation
2. Class Switch

Front 27

Daisy and other patients with hyper IgM syndrome caused by a mutation in AID do not seem to suffer from opportunistic infections, such as Pneumocystis carinii and Cryptosporidium, which are characteristic of the X-linked hyper IgM syndrome. Why?

Back 27

In hyper IgM: AID only affects the B cells, and not the T cells.

In X-linked hyper IgM: Defective CD40L affects T Cells, which affects the number of neutrophils, NK, and DC. Thus, patient is susceptible to opportunistic infections.

Front 28

Somatic Hypermutation?

Back 28

Nucleotide substitutions through the variable regions of the rearranged Ig heavy and light chain genes.

Front 29

Isotype Switching?

Back 29

Changes the isotype of the Ig, but not its antigen binding site.

Front 30

What's the WBC level of hyper-IgM patient?

Back 30

High neutrophils, low lymphocytes.

Front 31

Diversity during gene rearrangement is focused in what CDR domain of the Vh and Vl domain.

Back 31

CDR3.

Front 32

X-linked Hyper-IgM WBC Counts

Back 32

- WBC is lowered.
- low neutrophils (lack GM-CSF)
- normal lymphocytes
- elevated monocytes.

Front 33

Why do we normally wait for 14 days to test for antibodies?

Back 33

First time to get immunize – start making antibodies around 7-14 days. By 14 days, if we don’t see any antibodies, we’re not going to see any antibodies made.

Front 34

Cyclosporin A, a drug widely used for immunosuppression in graft recipients, also inhibits the transcription of the CD40 ligand gene. What does this imply for patients taking this drug?

Back 34

Have problems against pyogenic infections.

Front 35

What happen to B cells in germinal center?

Back 35

Proliferating B cells whose immunoglobulin genes are undergoing somatic hypermutation (changing their affinity).

Front 36

What's the purpose of somatic hypermutation?

Back 36

improve the binding affinity of the antibody molecule

Front 37

Four main processes of generating Antibody Diversity?

Back 37

1. There are multiple copies of the different v –gene segments
2. Combinatorial diversity – pairing of different Light and Heavy Chains.
3. Diversity is added at the joints between different segments as a result of recombination process
4. Somatic hypermutation introduces point mutations into rearranged variable region genes.

Front 38

3 functions of antibody.

Back 38

1. Neutralization
2. Opsonization
3. Activate Complement System

Front 39

What antibody is best at neutralization?

Back 39

IgA.

Front 40

Which antibody triggers allergy response?

Back 40

IgE

Front 41

Where else is CD40 can be found?

Back 41

CD40 is expressed not only on B cells but also on the surfaces of macrophages, dendritic cells, follicular dendritic cells, and mast cells.

Front 42

What are the primary lymphoid tissues?

Back 42

bone marrow and thymus

Front 43

What are the secondary lymphoid tissue?

Back 43

lymph node, spleen, GUT, tonsils, appendix

Front 44

What are two functions of spleen?

Back 44

1. lymphoid function is carried out in the white pulp. WBC’s gather to provide adaptive immunity.
2. filtration function is carried out in the red pulp.

Front 45

What are lymphocytes composed of?

Back 45

WBC: B cells, T cells, NK,

Front 46

T cells are activated by what cell?

Back 46

Dendritic cells.

Front 47

Patient with asplenia are susceptible to what kind of infection?

Back 47

encapsulated bacteria.

Front 48

Activation of naïve B cells requires help from what cell?

Back 48

CD4T cells.

Front 49

What happens in the white pulp of spleen?

Back 49

Contains WBCs. Site where lymphocyte responses to blood borne pathogens are made.

Front 50

What happens in the red pulp of spleen?

Back 50

Old RBCs are eliminated.

Front 51

Where do pathogens enter the lymph node?

Back 51

afferent lymphatic vessel

Front 52

Lymphocytes and blood enter the lymph node via what?

Back 52

Artery.

Front 53

Where do lymphocytes exit?

Back 53

Efferent lymphatic vessel?

Front 54

Where do blood exit?

Back 54

Vein.

Front 55

What are different WBC types?

Back 55

neutrophils, eosinophils, basophils, macrophages, dendritic cells

Front 56

What's serum?

Back 56

Plasma without clotting factors.

Front 57

What's plasma?

Back 57

Including clotting factors

Front 58

What's blood?

Back 58

plasma + formed elements, everything, WBC, RBC, platelets

Front 59

What's normal WBC count?

Back 59

4,500-10,000

Front 60

What's an immunogen?

Back 60

A substance (proteins, carbohydrate, nucleic acids, lipids) that elicits an immune response. Activates T cells/B cells/ other cells

Front 61

What's an antigen?

Back 61

A substance that binds to a specific antibody (antigen doesn’t stimulate antibody response).

Front 62

Can an antigen be an immunogen?

Back 62

No.

Front 63

What's the principle of immunization?

Back 63

To create a memory response.

Front 64

What's an adjuvant?

Back 64

A substance that enhances the immunogenicity of molecules (killed bacteria).

- Convert soluble proteins into particulate matter
- Add a bacterial constituent to boost innate immune system involvement

Front 65

What's a hapten?

Back 65

A hapten is a small molecule which cannot act as an antigen independently, but will stimulate the production of antibodies if it manages to find a carrier to bind to.

Front 66

What are hypervariable regions?

Back 66

Hypervariable regions make up the 3 loops at one end of the folded molecule which determines the “surface” of protein at that area. There are 3 HVR in both Heavy and Light chain variable regions.

Front 67

What are framework regions?

Back 67

Framework regions = b sheets that provide the structural framework of the domain. There are 4 of them. FR1-FR4.

Front 68

How does the antigen binding site form?

Back 68

The hypervariable loops from each of the VH and VL domains at the variable tip of the antibody molecule combine to form a single binding site for antigen. (They do this by forming a POCKET or CAVITY of surface complementarity to the antigen)/

Front 69

T/F. Amino acid differences and CDR/HV will drive the formation of different pockets.

Back 69

True.

Front 70

Is it the denatured or native form of protein that increases the immunogenicity?

Back 70

Denatured form (linear epitope)

Front 71

Forces that bind antigens to antibodies (non-covalent).

Back 71

Electrostatic
Hydrogen
Van der Waals
Hydrophobic interactions.

Front 72

Describe the method to produce monoclonal antibodies.

Back 72

1. B cells isolated from immunized animals
2. Immortalized by fusion with tumor cells
3. hybridoma cells that grow and produce antibodies
4. Individual hybridoma cells are separated.
5. identify the cells that produce the antibodies of desired specific.

Front 73

Why is HV4 unique in beta chain of TCR?

Back 73

It binds superantigens, which are products released by a certain type of bac and also some viruses; they can bind to HV4 region on beta chain of T cell receptor and bind to MHC molecule -> crosslinks the T cell and another cell together and by doing so, activates the T cell in a potent fashion -> rapid proliferation -> release cytokines -> exhaust and die. Pathogen can trick/modify immune sys, make it go crazy, strategic account to confuse the immune system—activates and kills T cell -> ”kill” immune system response mech

Front 74

Where does a superantigen bind?

Back 74

Superantigen binds to HV4 region on TCR and binds to a domain on the MHC; MCH:beta crosslink; superantigen NOT MHC restricted

Front 75

How many B and T cells are there in our body?

Back 75

B: 10^14
T: 10^18

Front 76

What are the driving force for antigen diversity in Ig and TCR?

Back 76

1. Somatic Recombination
2. Combinatorial paring (heavy and light)
3. Junctional Diversity
4. Somatic Hypermutation/Class Switch (Only in Ig)

Front 77

Why is a defect in CD40L significant?

Back 77

CD40L defect in T cells (X-linked Hyper IgM syndrome) will affect not only B cells but monocytes, macrophages and dendritic cells and these cells play a very important role in cell-mediated immune responses and preventing opportunistic infections. Macrophages produce the growth factor GM-CSF which is needed to produce neutrophils. The kid with AID only affected B cells. Thus both the X-linked Hyper IgM syndrome and AID children were highly susceptible to pyogenic infections, only the X-linked Hyper IgM syndrome kid was susceptible to opportunistic pathogens.