Pod: Antigen Recognition By T Cells

Front 1

List differences between TCR and BCR.

Back 1

1. TCR not secreted
2. TCR only has one receptor
3. TCR does not undergo class switch(no effector function), somatic hypermutation.
4. TCR generated in the thymus.

Front 2

What's the difference between TCR and BCR on binding antigens?

Back 2

TCR: bind to pieces of peptides presented by MHC molecules (class I and II).

BCR: bind to free intact peptide antigen, protein carbohydrates + lipids.

Front 3

Why do TCR has more J segments in its loci?

Back 3

Need diversity after antigen activation since there is no hypermutation(affinity maturation).

Front 4

Why don't TCR class switch?

Back 4

1. cytokines secreted are used for effector functions, no need to class switch.
2. TCR loci do not contain numerous C genes.

Front 5

The genes of α,β,δ,γ chain of TCR are located on which two chromosomes?

Back 5

α,δ: Chromosome 14
β: Chromosome 7
γ: Chromosome 7

Front 6

Descride the genectic make up of α and β chains of TCR.

Back 6

α chain: VJ region, one C segment
β chain: VDJ region, two C segments

Front 7

What happens if RAG genes are not expressed or defective?

Back 7

People develop SCID.
B and T lymphocytes are equally absent.

Front 8

What happens if CD3 complex is missing?

Back 8

Transport of TCR to the surface is defective and impaired signal transduction.

Front 9

How does TCR δ rearrangement resulting in 2 D-segments increases variability of δ chain?

Back 9

1. This increases the potential number of combination of gene segments.
2. Extra N nucleotide can be added at junction between 2D segments in addition to VD and V-DJ segments.

Front 10

Where are Tδ:γ cell dominated and its function?

Back 10

Epithelial tissue.
Innate immunity.

Front 11

Why are δ:γT cells involved in innate immunity, but not adaptive immunity?

Back 11

They are not associated with antigen presented by MHCs.

Front 12

Difference between the funcitons of Th1 and Th2 cells.

Back 12

Th1: activate macrophage by secreting cytokines IFN-γ, GM-CSF+IL3.

Th2: stimulate B cells to make antibodies.

Front 13

What virus infect CD4 T cells?

Back 13

HIV

Front 14

Differences of 2 classes of NHC molecules.

Back 14

MHCI: α1,2,3 (CH)and β2 microglobulin (CH15).
MHCII: α1,2, β1,2

Front 15

What makes up the binding groove in both MHC classes?

Back 15

MHCI: α1,2
MHCII: α1,β1

Front 16

What makes up the supporting domain of MHCI that CD8 binds?

Back 16

α3β2

Front 17

What makes up the supporting domain of MHCII that CD4 binds?

Back 17

α2β2

Front 18

The length of the peptide that MHCs bind is different. Specify the difference.

Back 18

MHCI: bind nonamers
MHCII: bind peptides of 13-25AA or longer.

Front 19

How does MHCI present intracellular antigens?
What chaperones are involved in this process?

Back 19

1. Proteasone degrade pathogenic protein into peptides.
2. peptide fragments transport into ER through TAP (ATP dependent).
3. α and β2 folding in ER.
4. α chain kept partially folded by Calnexin(calcium dependent lectin).
5. Calreticulin bind to α chain when β2 binds.
6. Tapasin binds to MHC and TAPI.
7. peptide bind the MHC groove.
8. MHCI:peptide shipped to the surface through Golgi.

Front 20

What is the funciton of TAP?

Back 20

Facilitate entry of broken peptide into ER.

Front 21

What is the function of Tapasin?

Back 21

Hold assembled MHC in proximity to TAP where peptides get in.

Front 22

What is the function of calnexin?

Back 22

Prevent α chain from folding completely before binding β2 microglobulin.

Front 23

What chaperone replaces calnexin when β2 microglobulin binds?

Back 23

Calreticulin.

Front 24

If TAP is missing, what condition results?

Back 24

Bare lynphocyte syndrome: no MHCI presented, no CD8 T cells, poor response to viral infection.

Front 25

How does MHCII present extracellular antigen and what chaperones are involved?

Back 25

1. endocytosis and form endocytic vesicles.
2. α,β chain associate with invariant chain in the ER.
3. MHCII delivered to endocytic vesicle where invariant chain is broken by cathepsin S, leaving only CLIP bound with MHCII.
4. HLA-DM removes CLIP and allow peptide bind with MHCII.
5. Transport to surface.

Front 26

What protein prevents MHCII from binding to intracellular antigens in the ER?

Back 26

The invariant chain.

Front 27

What is the function of HLA-DM?

Back 27

Allow MHCII bind with antigen in endocytic vesicle.

Front 28

How are 3 CDR loops arranged in TCR binding groove?

Back 28

CDR3 in the center, CDR1,2 in the periphery.

Front 29

Which CDR loop directly contact peptide antigen?

Back 29

CDR3.

Front 30

Which CDR loops contact MHC?

Back 30

CDR1,2

Front 31

Which class of MHC is secreted constitutively?

Back 31

Both. But MHC only expressed on professional APCs(DC cells, macrophages, and B cells) and epithelial cells of thymus.

Front 32

Which type of cell lack MHCI?

Back 32

Erythrocytes.

Front 33

What cytokines upregulates MHC expression?

Back 33

interferons.
IFN γ can induce MHC expression on cells normally don't have them.

Front 34

T cells stimulated by intracellular pathogens:
1. What class of T cell is stimulated?
2. What is the co-receptor?
3. What is the MHC molecule used for recognition?
4. What is the T cell effector function?

Back 34

1. CD8 T cell
2. CD8
3. MHCI
4. cytotoxic T cell: kill virus infected cells

Front 35

T cells stimulated by extracellular pathogens:
1. What class of T cell is stimulated?
2. What is the co-receptor?
3. What is the MHC molecule used for recognition?
4. What is the T cell effector function?

Back 35

1. CD4 T cell
2. CD4
3. MHCII
4. T helper cells: Th1: macrophage stimulation. Th2: B-cell stimulation

Front 36

Which MHCII HLA chain is monomorphic?
A. HLA-DP α
B. HLA-DQ α
C. HLA-DR α
D. HLA-DM α

Back 36

C

Front 37

Which domain within MHCII does CD4 bind to?

Back 37

β2 domain

Front 38

Which domain within MHCI does CD8 bind to?

Back 38

α3 domain

Front 39

What is maximum number of MHCII molecules that could be expressed?

Back 39

12

Front 40

What is maximum number of MHCI molecules that could be expressed?

Back 40

6

Front 41

What is maximum number of MHC molecules that could be expressed?

Back 41

18

Front 42

What are the anchor residues?

Back 42

The critical AA in the binding groove: anchor peptides to MHCs, same or similar to all peptides that bind to a given MHC.

Front 43

The genes for β2-microglobulin is located on which chromosome?

Back 43

Chromosome 15

Front 44

The genes for TAP1,2, tapasin in MHCI in which region of chromosome 6?

Back 44

Class II region

Front 45

The gene for the invariant chain is located on which chromosome?

Back 45

chromosome 5

Front 46

Expression of MHCII genes(HLA-DP, DQ, DR) and invariant chain is coordinated by which cytokine?

Back 46

IFN-γ

Front 47

What is the name of the transcriptional activator that is induced by IFN-γ to express MHCII genes(HLA-DP, DQ, DR)?

Back 47

MHC classII transactivator(CIITA)

Front 48

Class II MHC molecules all function inantigen presentation to T cell where as Class I molecules encompass a broader range of function. What are some these functions?

Back 48

1. uptake of IgG in the gut
2. regulation of iron metabolism
3. regulation of NK cells

Front 49

What is MHC restriction?

Back 49

Antigen-specific T cell response is restricted by the MHC type. A T cell that responds to a peptide presented by one MHC allotype with neither respond to another peptide bound by that same MHC allotype nor to the same peptide bound by a different MHC allotype.

Front 50

What's the difference between balancing and directional selection?

Back 50

Balancing selection: work to maintain genetic polymorphisms.
Directional selection:favors a single allele.

Front 51

What is interallelic conversion/segmental exchange?

Back 51

A small segment of one HLA allele replaced by homologous section of another allele (within the same gene).

Front 52

What are the two mechanisms that new MHC alleles are generated?

Back 52

1. interallelic conversion/segmental exchange
2. gene conversion: recombination between alleles of different genes.

Front 53

What does autologous mean?

Back 53

self-MHC isoforms

Front 54

What does allogenic mean?

Back 54

nonself-MHC isoforms

Front 55

What are alloreactive T cells activated by?

Back 55

peptide and allogenic MHC class I and II molecules present on healthy cells of other individuals.

Front 56

What is alloreaction?

Back 56

T cell response that attack the graft.

Front 57

What is alloantibodies?

Back 57

antibody raised in one member of the species against an allotype protein of another member of the same species.

Front 58

Role of NKT cells: (2)

Back 58

1. express cytokines upon interaction of baterial antigen
2. recognize lipid-containing antigens expressed by tumor cells.

Front 59

What does NKT cells recognize?

Back 59

nonpeptide antigens: glycolipid presented by nonpolymorphic CD1 molecules

Front 60

Do NKT cells form memory cells?

Back 60

No.

Front 61

Development of NKT cell in the thymus require_____.

Back 61

lysosomal glycosphingolipid (similar to glycoceramides in many bacteria)

Front 62

What is the role of CD1 molecules?

Back 62

present non-peptide antigens.

Front 63

δ:γ T cells:
A. are more important in adaptive immunity.
B. are the last T cell type to be produced in the thymus.
C. are the most abundant type of T cell in our bodies.
D. recognized intact antigens or pattern recognition.
E. recognize MHC molecules + antigenic peptide.

Back 63

D.

Front 64

How do TCRs differ from B cell receptors? TCRs____:
A. are soluble
B. do not undergo somatic hypermutation
C. lack heavy and light chains
D. recognize only carbohydrate antigens
E. recognize unprocessed antigenic peptides

Back 64

B.

Front 65

Antigen presentation involving class I MHC molecules do not involve:
A. proteasomes
B. TAP1,2
C. invariant chain
D. ER

Back 65

C.

Front 66

Antigenic presentation involving class II MHC molecules involves:
A. proteasomes
B. TAP1,2
C. invariant chain
D. ER

Back 66

C.

Front 67

Signal transdution by the TCR-CD3 complex is mediated MOST strongly by:
A. epsilon chain
B. delta chain
C. gamma chain
D. zeta chain

Back 67

D.

Front 68

The primary cause of allograft rejection of transplanted tissue is due to:
A. allelic exclusion
B. genetic hemogeneity
C. MHC polymorphism

Back 68

C.

Front 69

A child with a defiency in recombination activation gene (RAG-1 and/or RAG-2) would:
A. be able to reject a skin allograft.
B. be deficient only in B cells.
C. be deficient only in T cells.
D. lack both B and T cells.
E. make normal amount of IgG antibodies.

Back 69

D.