Exam 1 9/28 Kingsley Immuno Flashcards

1
Q

BCR recognizes ____ antigen

A

soluble

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2
Q

What proteins/components are involved with BCR Signal 1?

A

CD79 a/b or Ig-alpha and Ig-beta

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3
Q

What proteins/components are involved with BCR Signal 2?

A

CD21 recognizes C3d (breakdown of complement 3)

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4
Q

What is CD21?

A

complement receptor on B cell membrane

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5
Q

What is presented to T cells?

A

antigen-antibody complex via MHC I or II

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6
Q

Which cells are considered antigen presenting cells?

A

macrophages, B cells

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7
Q

A foreign antigen is presented to T cell (TCR) as:

A

non-self

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8
Q

True or false: TCR on T cells can recognize soluble antigens

A

False - this is for B cells
TCR recognizes only complexed/bound antigen by MHC

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9
Q

What protein is involved with signal transduction in TCR?

A

CD3

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10
Q

Which MHC does CD4 T-helper cells recognize?

A

MHC II
This is for exogenous or “found” antigens

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11
Q

Th1 is involved with what APC?

A

macrophages –> mainly involved with inflammation

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12
Q

Th2 is involved with what APC?

A

B-lymphocytes –> mainly involved with humoral response

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13
Q

Clonal expansion

A

Clonal selection –> that B cell starts to divide rapidly and differentiate into plasma cells which secrete antibody
- memory B cells retain BCR

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14
Q

Clonal expansion allows for what kind of response?

A

2ndary anamnestic

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15
Q

T-dependent responses

A
  1. most antigens, usually complex proteins
  2. multiple, different determinants
  3. efficient response, memory –> B memory cells formed
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16
Q

T-independent responses

A
  1. polysaccharides, LPS, nucleic acids
  2. repeated determinants, usually IgM response
  3. weak, no memory
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17
Q

Immunologic memory definition

A

B and T cells following activation; larger number of existing cellls with specific receptor for particular antigen

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18
Q

One activated B cell can produce up to how many plasma cells?

A

4000

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19
Q

B cell surface Ig - high or low?

A

High

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20
Q

Plasma cell surface Ig - high or low?

A

Low

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21
Q

Does B cell have surface MHC II?

A

Yes

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22
Q

Does plasma cell have surface MHC II?

A

No

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23
Q

Do B cells secrete Ig?

A

No

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24
Q

Do plasma cells secrete Ig?

A

Yes

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25
Q

Is there growth in B cells?

A

Yes

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26
Q

Is there growth in plasma cells?

A

No

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27
Q

Can B cells undergo isotype (class) switching?

A

Yes

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28
Q

Can plasma cells undergo isotype (class) switching?

A

No

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29
Q

Primary antibody produced

A

IgM

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30
Q

Primary antibody production lag time

A

7-10 days

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31
Q

Secondary response activates:

A

memory B cells (have IgM); rapid shift to produce IgG

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32
Q

Secondary response lag time

A

1-4 days

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33
Q

Affinity maturation

A
  1. IgG is formed due to class switching after secondary response, has higher affinity for antigen than IgM
  2. highest affinity B cells selected by binding to antigen on follicular dendritic cells
34
Q

Lag phase

A

time between antigen exposure and antibody response

35
Q

Which part of the antibody changes during class switching?

A

Only the CH. VH and light chain do not change

36
Q

When class switching occurs, what is preserved?

A

The idiotype (antigen combining site)

37
Q

What is the directionality of class switching?

A

Unidirectional (ex: IgE can’t go to IgM, IgG, or IgA)

38
Q

IgG class switching requirements

A

IL-4 and IFN-gamma

39
Q

IgA class switching requirements

A

IL-4 and TGF-B

40
Q

IgE class switching

A

IL-4 by itself

41
Q

Memory B cells are activated (faster/slower) than naive B cells, leading to:

A

faster; shorter lag phase

42
Q

Where are memory IgA cells/plasma cells formed?

A

Near mucosae

43
Q

Where do B and T cells get activated?

A
  1. external facing mucus-lined surfaces (MALT, GALT)
  2. lymphatic drainage sites (lymph nodes)
44
Q

Where are B cells found in lymph nodes?

A

cluster (follicle) cortex

45
Q

Where are T-cells found in lymph nodes?

A

Paracortex/parafollicular cortex (either name)

46
Q

What happens in the lymph node when antigen enters afferent lymph vessel?

A

Germinal center develops; B and T cells found in secondary follicle

47
Q

Waldeyer’s ring is composed of:

A
  1. pharyngeal tonsil/adenoid
  2. 2 tubal tonsils
  3. 2 palatine tonsils
  4. lingual tonsil
48
Q

What is the function of the germinal center?

A

Active site of B cell proliferation and differentiation within secondary follicles

49
Q

B cell doubling time

A

6 hours

50
Q

True or false: class switching occurs in germinal center

A

True

51
Q

Antibody molecules include a ____ ____ set of antigen-binding sequences

A

potentially unlimited

52
Q

Somatic hyper mutation and recombination is also known as:

A

variable domain recombination (DNA rearrangement) - somatic recombination of VDJ DNA

53
Q

What areas of the body does somatic recombination occur?

A

Bone marrow and thymus

54
Q

Where does somatic recombination occur?

A

Hypervariable regions of BCR and TCR

55
Q

X-linked severe combined immunodeficiency (XL-SCID) - what is the cause?

A

IL-2 receptor has reduced function; required for B and T cell development and proliferation (in the chart, says there is much less T cells)

Leads to non-functional IL-7 function in the thymus

56
Q

Who is more likely to be affected by XL-SCID?

A

Males - since it is X-linked

57
Q

What is the cause of DiGeorge syndrome?

A

22q11.2 deletion syndrome; thymic aplasia

58
Q

DiGeorge syndrome is mainly acquired via:

A

de novo deletion

59
Q

Main symptoms/clinical manifestations of DiGeorge syndrome

A

Cleft palate, other craniofacial disorders

60
Q

What gene is affected in DiGeorge syndrome?

A

TBX1 - responsible for pharyngeal pouches

61
Q

“complete” depletion of TBX1 results in:

A

Absence of thymus in DiGeorge syndrome

62
Q

Pharyngeal pouch 3

A

Thymus

63
Q

Pharyngeal pouch 4

A

Superior parathyroid gland

64
Q

Bare lymphocyte syndrome 1 (BLS1) is known as:

A

MHC1 deficiency

65
Q

Bare lymphocyte syndrome 1 (BLS1) is caused by:

A

Mutations in TAP1 - does not allow normal protein complex with MHC1

66
Q

Bare lymphocyte syndrome 2 (BLS2) is known as:

A

MHC II deficiency - does not allow foreign antigens to complex with MHC II

67
Q

MHC deficiency means that you cannot:

A

Class switch/clonal expansion

68
Q

What happens to CD8/CTL in BLS1?

A

not able to detect pathogens; leads to intracellular parasites and viral infection

69
Q

BLS II is a form of:

A

SCID –> TH1 and TH2 responses are non-functional

70
Q

Heterotaxy syndrome

A

Internal thoracic-abdominal organs exhibit abnormal arrangements across left-right axis

71
Q

Asplenia heterotaxy syndrome

A

Missing spleen entirely

72
Q

Spleen is a major site for:

A

Antibody production

73
Q

Polysplenia heterotaxy syndrome

A

Multiple small accessory spleens with reduced function; other organs like thymus may be affected

74
Q

What disease do you see a 350-fold increased risk of bacterial sepsis?

A

Isolated congenital asplenia

75
Q

What bacteria are commonly found to cause infection in isolated congenital asplenia?

A

Polysaccharide encapsulated bacteria

76
Q

Pemphigus antibody/targeted structure

A

Auto-antibodies IgG against desmoglein-3 of desmosome

77
Q

Pemphigoid targeted structure

A

autoantibodies to BP-1 of BMZ, hemidesmosome

78
Q

Linear IgA targeted structure

A

Linear IgA deposition in BMZ

79
Q

EBA autoantibody/targeted structure

A

Auto-immunity IgG develops against Type VII procollagen

80
Q

Pemphigoid is characterized as:

A

cicatricial (mucous membrane) - oral

81
Q

Goodpasture syndrome

A

Autoantibodies to alpha-3 subunit of Type IV collagen