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Immunology 1 Answers

1. B

2. TLR 2 = LPS
TLR 3 = dsRNA
TLR 4 = Peptidoglycan
TLR 5 = Flagellin
TLR 7 = ssRNA
TLR 8 = ssRNA

3. False. They are present on DCs, neutrophils, B cells and a wide range of other
immune cells

4. C

5. NOD-like receptors, RIG-1 like helicases and Cyclic GMP-AMP synthase are all pattern
recognition receptors that are able to identify pathogens present within the cytosol
of a cell.

6. Sensory protein: NLR3, detects the ligand

Adaptor protein: ASC, middle molecule
Effector protein: caspase-1, is able to induce cleavage

7. IL-1 and IL-18

8. Signal 1 = detection of pathogen or pathogen related molecule by PRRs on cells

Signal 2 = actual activation, formation and activation of the inflammasome

9. B

10. Defensins, histalins. Induced by cytokines such as IL-1 and TNFs

11. IL-17 regulates neutrophil production through activating G-SCF

12. Immature dendritic cells are found in the periphery and have an increased ability to
uptake antigens and a decreased ability to present them. The reverse is true for
mature dendritic cells where MHC I and MHC II are expressed in higher levels.

13. Alum adjuvant is used to activate the NLR3 inflammasome. It is the most commonly
used adjuvant in humans and induces strong humoural immunity and Th2
dependent immunity.

14. False. Only T cells can recognise denatured protein antigens.

15. Transplant grafts are rejected when MHC molecules do not match.

16. Self-MHC restriction is the requirement that APCs express MHC molecules that T
cells recognise as self in order for them to respond to that Ag presented. T cells will
only recognise Ags presented on self MHC molecules.

17. B

18. MHC class I =

MHC class II =

19. A

20. MHC class I = endogenously, from the cytoplasm, nucleus or ER

MHC class II = endogenously (secreted only) or exogenously

21. MHC class I =

22. MHC class II =

23. Dendritic cell licencing occurs when CD4+ T helper cells attempt to aid CD8 T cells
through their (CD4+) interaction with DCs. CD4+ Th cells bind to DC and cause them
to upregulate co-stimulatory moelcules such as CD80/CD86 and downregulate
inhibitory molecules such as PD-1L so that they are better able to engage with CD8+
T cells.

24. False.

25. In the periphery.

26. Cross presentation is the ability of a DC to present exogenous antigens via the MHC
class I pathway. It is necessary for when a pathogen does not directly infect a DC but
instead infects another susceptible host cell. Only CD8+ and CD103+ DCs can carry
out cross presentation.

Cell B cell T cell
Ligand:Receptor Antigen: surface Ig (BCR) Antigen-MHC: TCR
Antigenic epitope Confirmation and linear Linear fragment
Response Free protein/response Fragment of
glycoprotein to MHC 1 or
Affinity of antigen binding 10-11 10-7
Estimated diversity About 1011 1016
28. D

29. The heavy chain

30. Combinatorial diversity = the random recombination of V-D-J or V-J segments to

form the TCR
Junctional diversity = the random addition or subtraction of nucleotides during the
recombination process

31. True

32. 1 and 3

T cell type T cells T cells
Ag-receptor configuration CD3 complex and TCR CD3 complex and TCR
Theoretical receptor # 1015 1020
Antigen recognition Peptide-MHC (restricted Protein and non-protein
to peptides)
MHC restriction Yes Rare
Phenotype CD4+ or CD8+ CD4-/CD8-, iLELs are
CD8+ ()
Frequency 65-75% blood 1-5% (blood), 25-60%
Effector capacity CTLs and cytokine release CTLs and cytokine release
Function Immune protection, Immunoregulation,
pathogen eradication immunosurviellance

34. Lck is a downstream kinase that functions in signalling cascades that result in the
phosphorylation of PLC1 and activation of Ras, MAPK pathways

35. Positive selection is the process by which low-affinity, anti-self T cells are selected
for maturation into nave T cells. It ensures that TCRs are usable and will not be self-
reactive leading to autoimmune pathologies. Negative selection ensures that self-
reactive TCRs that have high affinity reactions with self-MHC molecules are deleted
from the repertoire. These two processes maintain central tolerance?

36. AIRE (autoimmune regulator) is expressed in medullary epithelial cells and allows
thymic expression of peripheral tissue (e.g. Insulin) antigens on MHC. It has an
important role in central tolerance.

37. Th1 = stimulated by IL-12 (STAT-4), differentiates into Th1 via STAT-4 and STAT-1 to
produce IFN- (STAT-1) and TNF. Is important in intracellular and protozoan
infections and acts by stimulating macrophages.
Th2 = stimulated by IL-4 (STAT-3, STAT-6), differentiates into Th2 via STAT-3 and
STAT-6 and produces IL-4, IL-5 and IL-13. Is important in helminth immunity and acts
via causing mast cell degranulation, antibody production, eosinophil and
macrophage activation and mucosal secretions within the gastrointestinal tract.
Th17 = stimulated by IL-6 (STAT-3), TGF- (RORT) and IL-1 to differentiate into
Th17 and produce IL-17 and IL-22. Has important role in immunity against
extracellular and fungal infections and causes an increase in barrier function of
tissue cells as well as immune cell recruitment that results in inflammation.

38. Signal 1 = TCR interaction with MHC II class molecule on APCs

Signal 2 = interaction with CD28 of T cell with CD80/CD86 of APCs
Signal 3 = cytokine release to determine differentiation of cell

39. Cross regulation occurs when one CD4+ T helper cell subset is formed and
subsequently inhibits the formation of another subtype. For example, the
differentiation of Th2 cells causes the release of IL-10 to prohibit the formation of
Th1 cells.

40. Th1 = CXCR3, Th2 = CCR4, Th17 = CCR6

41. See above.

42. CD8+ CTLs are activated in the lymph nodes when APCs present an antigen bound to
the MHC class I molecule. This presentation in conjunction with the interaction
between CD28 on the T cell with CD80/86 on the APC results in the activation of the

43. CD4+ T cells interact with APCs via their CD40L and the CD40 receptor on APCs to
result in the increased signalling with APCs that promotes their interaction and
activation of CD8+ T cells

44. A

45. True. If a CTL has already been activated it does not require a second signal from co-
stimulatory molecules.

46. Perforin: forms an aqueous pore within the lipid membrane of the target cell to
allow the delivery of granzymes.
Granzymes: induces apoptosis within the target cell by cleaving and activating
caspases with in the cell.

47. TNF/, IFN-

Activating receptors Inhibiting receptors
CD16 = for IgG (ADCC) KIRs
NKG2D = ligands present on stressed CD94/NKG2A = non classical MHC I
cells LIRs/ILT-2 = bind MHC molecules
49. False. Antigen specificity doesnt increase with the maturation of T cells. Only B cells
can increase their antigen specificity.

50. CD3 = n/a

= n/a
PD-1 = PD-1L
CD28 = CD80/CD86
CTLA-4 = CD80/CD86


52. c-SMAC (central) = TCR, CD4/CD8, CD28, enzymes

p-SMAC (peripheral) = ligands

53. TCR engages with MHC-bound antigen which causes the recruitment of Lck within
the T cell. Lck is able to phosphorylate the ITAM present on the CD3 receptor as well
as the 3 ITAMs on the chain. This phosphorylation causes the recruitment of ZAP-
70 which results in downstream signalling events that lead to calcium signalling and
gene expression/metabolic changes.

54. CTLA-4 is induced on conventional T cells and constitutively expressed on T

regulatory cells. It has a higher affinity for CD80/CD86 found on APCs than the CD28
molecule does. Its binding to the co-stimulatory molecules on APCs prevents the
second signal needed for T cell activation to successfully occur.

55. False. CD40L is found on T cells and it binds to CD40 receptor on APCs which results
in the production of IL-12 that consequently enhances T cell stimulation.

56. T cell activation events

a. Immunological synapse formation = makes cell immobile
b. CD68 expression = ensures T cell stays within the lymph node
c. IL-2 release and IL-2R = signals cell to grow and proliferate
d. CD40L expression = engages with APCs to increase co-stimulation and
e. CTLA-4 expression = to regulate the immune response

57. IL-2, IL-4, IL-7, IL-9, IL-15, IL-21

58. Central memory T cells (Tcm) = produce cytokines, able to recirculate but found in
lymphoid tissue generally.
Effector memory T cells (Tem) = circulate through system, ready for rapid
proliferation in response to re-encountering antigen.
Resident memory T cells (Trm) = cannot recirculate and remain in peripheral tissue.
Repsonsible for surveillance and rapid response.

59. True.

60. ILC1 = produce IFN- and TNF, transcription factor is T-bet, important in clearance of
viral and intracellular bacteria and implicated in Crohns disease. Found in the liver
and salivary glands.
ILC2 = produce IL-4, IL-5, IL-13, transcription factor is ROR and GATA-3. Important in
helminth infections, wound repair and homeostasis. Implicated in hayfever, fibrosis,
eczema and asthma. Found in the skin, lungs and adipose tissue.
ILC3 = the most characterised group, produce IL-17 and IL-22, transcription factor is
RORT. Has many functions including homeostasis in the caecum, T cell tolerance to
bacterial antigens, DC tolerance (via GM-CSF) in the intestine, contain intestinal
infection and promote IgA production. Implicated in colitis and psoriasis. Found in
the gut mucosa

61. True.


63. Initiation clonal expansion Contraction Memory/maintenance

64. B and C

65. Phenotypic changes, metabolism changes, Transcriptional profile changes,

Epigenetic changes.

66. Central memory T cells (Tcm): circulate through lymphoid tissues and have are highly
Effector memory T cells (Tem): circulate through non-lymphoid tissues and have
enhanced effector funcitons.
Resident memory T cells (Trm): do not circulate, are in resident tissue ready to re-
encounter pathogen for quick adaptive immune response.

67. False.

68. True.

69. Pleiotropic: can act on different cells

Redundancy: more than one cytokine has the same action on the same cell
Antagonistic: can inhibit other cytokine effects
Synergistic: have a cooperative effect

70. C. IL-7 is required for lymphocyte development and IL-15 for NK development
71. Type 1 and 3 IFNs = are important in anti-viral immunity, produced by innate and
tissue cells.
Type 2 IFNs = are important in intracellular bacteria and parasitic infections and are
produced by activated lymphocytes.
All types of IFNs utilise the JAK/STAT signalling pathway. JAK recruits STAT which is
then phosphorylised and leaves to dimerise in the cytoplasm of the cell STAT
enters nucleus and transcribes cytokine responsive genes.

72. IL-1Ra is a naturally occurring cytokine that is produced in high concentrations

during inflammation. Its ratio with IL-1 influences disease severity due to its
regulatory role by blocking IL-1RI receptors so that IL-1 cant activate them.

73. IL-10 Inhibits DC maturation and limits the ability of macrophages to kill intracellular
organisms. Supress Th1 responses to inhibiton of IL-12 production by DCs and
macrophages, acts directly on pro-inflammatory Th17 cells.

74. False. Chemokines are broken into 4 families.

75. Integrins and selectin ligands present on endothelial cells. Selectin and integrin
ligands present on leukcotyes?
Chemokine release causes increase in affinity of integrins present on cell surfaces for
their ligands. This mediates the adhesion of cells to other cells and is essential for
recruiting lymphocytes to the site of injury.

76. Oposinisation
Cell lysis
Clearance of immune complexes
Enhancement of Ab-Ag formation.

77. A C1 inhibitor can inhibit the formation of C1q. Absence of this inhibitor leads to
increased inflammation due to increase C2a and C4b, swelling of the face and gut.

78. False. CD59 blocks C9 binding and MAC formation, in its absence, a decrease in
sensitivity to complement lysis of RBC and haemolytic anaemia is seen.

79. IgG2

80. FcyRIIB receptor

81. Increase in efficiency of phagocytosis, activation of phagocyte oxidase and ROI

production, cytokine secretion and other anti-microbial peptides.

82. A non-functional NAPDH oxidase, neutrophils and macrophages. Failure to produce


84. A

85. C

86. True.

87. 10^15

88. To cut the strand adjacent to the heptamer nonamer sequences to allow for VJ and
VDJ joining.

89. Artemis opens up the hairpin loops that form on the ends of the cleaved strands in
order to allow for TdT do add/subtract nucleotides to the regions between VJ and
VDJ to increase junctional diversity.

90. Choice of V, D and J gene segments used

Random removal and addition of nucleotides to the coding joints
Combination of successful IgH rearrangement with a successful IgL rearrangement.

91. B

92. It allows an increase in affinity binding to its antigens. The binding interaction
between 1 IgM and its antigen is of low affinity, so by increasing the number of IgMs
within a structure you increase the binding affinity.

93. If Ab/Ag binding was of high affinity there would be binding that would occur with
innate cells in the context of no infection.

94. False. No receptor has specificity for IgM

95. Macrophages, neutrophils, eosinophils

96. AID is an enzyme that is active in isotype switching and somatic mutation. It converts
C to U (likes AGCT sequences) and U is subsequently removed from the sequence by
DNA repair machinery. This creates as double stranded break in the sequence (highly
unstable) which is then repaired. The repairmen process results in a recombined
strand that is different to what the beginning product.

97. Somatic mutation occurs in the germinal centre and is result of competition for
affinity between rapidly proliferating B cells. Variable regions mutate but C do not.
AID is required and induces mutations via the C U in Ig. Error prone DNA repair
occurs in 3 ways: UNG enzyme, passive mutations, UG mismatch recognised by
mismatch repair system = errors nearby.
98. Anergy, deletion, suppression

99. CD59 blocks C9 and subsequently the formation of the MAC. C1 inhibitor blocks
complement activation at the C1 stage.

100. IL-1Ra is a constitutively expressed cytokine that binds to the IL-1RI receptor
and provides an inhibitory signal to that cell. It takes up binding sites that would
otherwise be used by IL-1 for activating signals. IL-1 has inflammatory actions so by
competing with it for its receptor, IL-1Ra prevents inflammation. The ratio of IL-1 to
IL-1Ra is responsible for disease outcome.

101. SCOS are protein inhibitors of the JAK-STAT pathways linked to cytokine

102. B

103. True