Immunology Flashcards

1
Q

What do mycobacteria infect?

A

They infect antigen presenting cells

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2
Q

Where are the blood tissue barriers and hence immune privileged tissues?

A

Blood-brain barrier
Blood-ocular barrier
Blood-testis barrier

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3
Q

What are warm antibodies?

A

IgG

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4
Q

What are cold antibodies?

A

IgM

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5
Q

Which antibodies form monomers?

A

IgG
IgE
IgD

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6
Q

Which antibodies form dimers?

A

IgA

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7
Q

Which antibodies form pentamers?

A

IgM

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8
Q

Which antibodies cannot cross the placenta?

A

IgM

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9
Q

Give examples of uses of passive immunity

A

Anti-venins
Pooled Ig for immune deficiencies
To prevent rhesus disease

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10
Q

What is caused by the measles vaccine?

A

SSPE

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11
Q

What is the marker for memory b cells?

A

CD27

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12
Q

What is the marker for memory T cells?

A

CD45

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13
Q

What are the 6 types of vaccine?

A
Killed whole pathogen
Live attenuated
Sub unit
Synthetic
Toxoid
Conjugate
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14
Q

What is an attenuated pathogen?

A

Made unable to grow in the human body or grow slowly

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15
Q

What is the function of adjuvants?

A

Increase the immune response

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16
Q

What adjuvant is used in viral vaccines?

A

IL33

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17
Q

How does HIV enter T cells?

A

Gp120 on HIV binds CD4

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18
Q

What are the problems associated with a HIV infection?

A

Antibodies against gp120 can enhance infection in macrophages

Antigenic drift

Initial infection is transmitted by infected cell not by free virus

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19
Q

What are 5 types of immunodeficiencies?

A
X linked agammablobulinemia
ADA SCID
MHC deficiency
Ig deficiency
T cell deficiency
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20
Q

What are treatments for immunodeficiencies?

A
Prophylactic antibiotics
PEGAylated ADA injections
HSCT
Gene therapy
Pooled gamma globulin
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21
Q

What mutation is associated with x linked agammaglobulinemia?

A

Btk which causes mutational arrest of B cells

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22
Q

What are 3 contributory causes of MS?

A

Vitamin D
EBV infection
Genetics

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23
Q

What gene is associated with MS?

A

HLA-DRB1

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24
Q

What are the antigens in MS?

A

MBP
MOG
PLP

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25
Q

What is the pathophysiology of MS?

A

CD4 T cells are activated by APC, they express VLA4 so can cross the blood brain barrier. T cells cause inflammation with leads to demyelination. Increased levels of IgG and leukocytes are found in the cerebrospinal fluid

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26
Q

How does a decrease in vitamin D cause MS?

A

Increases inflammation. Less vitamin D = more Th1 response

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27
Q

What treatments are available for MS?

A

Interferon beta (inhibits IFN gamma)

Corticosteroids

Antibody therapies (rituximab against b cells and natalizumab against VLA4)

Methrotrexate

Cyclophosphamide (promotes Th2 response and is toxic to proliferating cells)

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28
Q

What does the classical complement system recognise?

A

Antibody:antigen complexes

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29
Q

What does the MBP/lectin system recognise?

A

Sugar residues

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30
Q

What does the alternative pathway recognise?

A

Pathogen surfaces

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31
Q

What is the result of all 3 pathways?

A

Production of C5 convertase and MAC

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32
Q

Why does complement have to be regulated?

A

To prevent it attacking host membranes

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33
Q

What regulates complement?

A

C1 disrupters
C3 convertase disrupters
MAC inhibitors

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34
Q

Common pathway

A

C3 + C3 convertase = C5 convertase

C5 convertase is cleaved to form C5a and C5b. C5b directs the MAC.

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35
Q

MAC

A

C5b binds C6 and C7 which then binds to the pathogen membrane. C8 binds to the complex and inserts into the membrane. Many molecules of C9 bind to form a pore

36
Q

What activates phagocytes?

A

Complement
Antigen antibody complexes
Stranger signals
Danger signals

37
Q

Example of stranger signal

A

Bacterial flagella

38
Q

Example of danger signal

A

Uric acid from breakdown of purines in dying cells

39
Q

How do phagocytes kill bacteria?

A

Respiratory burst

40
Q

Where in a phagocyte are bacteria digested?

A

Phagosomal lysosomal compartment

41
Q

What is respiratory burst?

A

How phagocytes kill bacteria. It consumes oxygen and is initiated by NADPH oxidase

42
Q

How does the respiratory burst kill bacteria?

A

Production of ROS

43
Q

What diseases are associated with phagocytosis?

A

Chediak higashi syndrome
Leukocyte adhesion deficiency
Chronic granulomatous disease

44
Q

What is chediak higashi syndrome?

A

Improper phagosomal lysosomal function

45
Q

Leukocyte adhesion deficiency

A

Prevents phagocytes migrating

46
Q

Describe the structure of an antibody

A

Two light chains
Two heavy chains
Variable region with 2 antigen binding sites
Constant (Fc) region

47
Q

What are the types of immunoglobulin in order of abundance?

A

IgG IgA IgM IgD IgE

48
Q

Where are IgM and IgG found?

A

Serum

49
Q

Where is IgA found?

A

Mucosa

50
Q

Where is IgD found?

A

Restricted to the B cell membrane - is a B cell receptor

51
Q

What is the role of IgE?

A

Activates mast cells

52
Q

How is antibody diversity achieved?

A

Combinatorial diversity

53
Q

How are antibody light chains produced?

A

Combining V J C gene segments

54
Q

How are antibody heavy chains produced?

A

Combining VDJC gene segments (D = diversity)

55
Q

What controls gene rearrangement in immunoglobulin?

A

Rag 1 and rag 2 recombinase

56
Q

What do mutations in RAG genes lead to?

A

Omenn syndrome (severe immunodeficiency)

57
Q

How do B cells change the sub-type of antibody?

A

Class switching

58
Q

What is the role of AID

A

Controls somatic hypermutation in antibody genes. This can increase antibody affinity

59
Q

Describe MHC I antigen processing

A

Cytosolic proteins are degraded by the proteasome, transported to ER by tap, trimmed by ER peptidases, loaded onto the binding groove of MHC I which is then trafficked to the cell membrane

60
Q

What are CD1 molecules?

A

Bind non-self glycolipids and present them to T cell receptors on NK cells

61
Q

Describe MHC class II antigen processing

A

MHC II assembles as heterodimers in the ER. Invariant chain binds to the peptide binding groove. Transported to an endocytic vesicle which is acidified to cleave invariant chain to CLIP. Engulfed pathogen proteins are degraded by the proteasome and bind to the peptide binding groove thanks to HLADM. MHC is then trafficked to the cell surface.

62
Q

Where are T cells selected?

A

Thymus

63
Q

What are CD4 T cells?

A

Helper T cells (provide help to B cells)

64
Q

What are CD8 T cells?

A

Kill virally infected cells

65
Q

What are Tregs

A

T cells which modulate the immune system

66
Q

What happens when the T cell receptor is stimulated?

A

The T cell divides to produce clones with the same T cell receptor specificity

67
Q

T cell receptor genes

A

VJC for the alpha chain

VDJC for the beta chain

68
Q

How are T cell receptor genes rearranged?

A

Rag dependent mechanism

69
Q

What coreceptor does the T cell receptor require?

A

CD3

70
Q

What co receptor does the B cell require?

A

Ig alpha beta heterodimer

71
Q

Which cytokine stimulates T cell clone expansion?

A

IL2

72
Q

What is the role of interferon gamma?

A

Suppresses viral infection of cells

73
Q

What releases IL1 and TNF alpha

A

Macrophages

74
Q

TNF alpha receptor pathway

A

Signals through MAP kinase or ERK kinase to activate NFkB

75
Q

Il1 signalling pathway

A

Signals through MyD88 and IRAK kinase

76
Q

How do T reg cells maintain peripheral tolerance?

A

Secrete cytokines that inhibit autoreactive T helper cells

77
Q

Autograft

A

Transplant from recipients own tissues

78
Q

Allograft

A

Transplant from non-identical members of the same species

79
Q

Isograft

A

Transplant from genetically identical individuals (monozygotic twins)

80
Q

Xenograft

A

Transplant from different species

81
Q

Hyperacute rejection

A

Rejection within minutes of transplant

82
Q

Acute rejection

A

Rejection within 2 weeks of transplant due to MHC mismatch

83
Q

Chronic rejection

A

Months to years after transplant, mechanism unknown

84
Q

Which immunosuppressant drugs are used in transplants?

A

Cyclosporin A
Rapamycin
FK506

85
Q

How do immunosuppressant drugs for transplant work?

A

Block IL2 production

Block T cell cell cycle