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Immunology > Prep2 For Exam > Flashcards

Prep2 For Exam Flashcards

1
Q

What are the types of allograft rejection?

A
  1. Hyperacute (antibody-mediated); 2. Acute vascular (antibody-mediated); 3. Cellular; 4. Chronic (antibody-mediated)
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2
Q

What causes the development of anti-HLA antibodies?

A

Pregnancy, blood transfusion, previous transplant

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3
Q

How does hyper acute graft rejection occur?

A

Antibody recognition of antigen on the endothelial surface occurs, followed by complement fixation and activation of the coagulation cascade

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4
Q

How does acute cellular rejection of a transplantation occur?

A

Caused by effector T cells responding to HLA differences and minor histocompatibility antigens between donor and recipient

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5
Q

How do steroids affect transplants?

A

Immunosuppressive; change patterns of gene expression

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6
Q

What does cyclosporine do?

A

Calcineurin inhibitor (therefore inhibiting T-cell activation)

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7
Q

What does Rapamycin do?

A

MTOR inhibitor, therefore having a sparing effect on Treg cells

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8
Q

How is GVHD beneficial?

A

It can help engraftment and prevent the relapse of malignant disease

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9
Q

How can GVHD occur even when HLA match is identical?

A

Recognition of minor histocompatibility antigens (peptide polymorphisms)

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10
Q

How is organ rejection prevented?

A

Identical twins, immunosuppressive drugs, induce tolerance

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11
Q

What are the stages of the development of autoimmune disease?

A
  1. Healthy w/ genetic susceptibility/environment; 2. Healthy w/ autoimmune response but no tissue injury; 3. Disease w/ autoimmune-driven inflammation and tissue injury
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12
Q

Regarding immunology, what do identical twins share? Not share?

A

They share MHC/HLA, but they are NOT identical in their T and B cell repertoires

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13
Q

What is APECED?

A

Inadequate expression of self-peptides in thymus resulting in failure of negative selection to remove self-reactive T cells; symptoms include hypothyroidism, alopecia, vitiligo, malabsorption, hepatitis, etc; mainly organ-specific disease

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14
Q

What is IPEX?

A

Defect in FOXP3 gene, resulting in deficiency of Tregs; symptoms are somewhat similar to APECED, mainly organ-specific diseases

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15
Q

What are the differences between MHC Class I associated disease and MHC Class II associated disease?

A

MHC Class I: no autoantibodies, CD8 T cell pathogenesis; Class II: autoantibodies reflecting CD4 T cell help - injury may be from auto antibody or CD4 T cell

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16
Q

How does MHC affect Type I diabetes?

A

HLA-DQ8 aspartic acid is replaced by alanine, which can’t form salt bridge, permitting the positive thymocytes selection of a potentially pathogen T cell pop and failure to induce T regs

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17
Q

Define: ANA

A

SLE patients will have autoantibodies that react w/ nuclear antigens at a dilution of 1:160; there is a diversity of ANA patterns

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18
Q

Which populations have increased autoantibodies?

A

Women, older people (increases w/ age), African Americans

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19
Q

Define: Immune Tolerance

A

Discrimination between non-self and self and between harmless and dangerous

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20
Q

Define: Affinity

A

Binding strength of one receptor to one ligand

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21
Q

Define: avidity

A

Aggregate binding strength of multiple ligands

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22
Q

What kind of avidity do you want in T cell activation?

A

Low-to-intermediate

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23
Q

What is AIRE?

A

Autoimmune regulator gene that is highly expressed in thymocytes epithelium; encodes a transcriptional activator and induces expression of “ectopic” self proteins

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24
Q

What happens if you have Signal 1 without Signal 2?

A

Anergy occurs - a state of long-term hypo responsiveness to all further antigenic stimulation

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25
Q

What is activation-induced cell death (AICD)?

A

Elimination of clonally expanded effector T cells in the “terminal phase” of antigen response; cell death is apoptotic - largely FAS mediation; inappropriate AICD may result in pathological T cell loss

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26
Q

What does CTLA-4 do?

A

Natural break on T cell response - binds CD80/86 w/ higher avidity than CD28, delivers an inhibitory signal to responder T cell

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27
Q

What does PD-1 do?

A

Inhibits TCR-trigger signaling; expressed on CD4 and CD8 T cells within 2 hours of activation; decreases NF-AT activation and Ca2+ influx

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28
Q

What are the differences between CTLA-4 and PD-1?

A

PD-1 much faster (CTLA-4 is 4-5 days vs. 2 hrs); PD-1 is a stronger inhibitor; PD-1 favors cell death, while CTLA-4 has no effect on anti-apoptotic factors

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29
Q

What happens if you have mutations in PD-1?

A

Risk for SLE, MS, RA, T1DM

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30
Q

What prevents uncontrolled T cell activation?

A

Anergy (requirement for costimulation); Ignorance (sequestration of some antigens); AICD (vulnerability of T cells to apoptosis)

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31
Q

What does CD25+ mean?

A

10% of circulating CD4+ cells express high levels of CD25 - prevents secretion of IFNg, IL2, constitutively expresses CTLA-4 and PD-1

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32
Q

What does FoxP3 do?

A

Proposed “master controller” for Treg program

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33
Q

What are the mucosal tissues of the human body?

A

GI tract; respiratory tract; genital tract

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34
Q

Where are the majority of Ig in healthy individuals produced?

A

The mucosal immune system - secreted IgA>all other Ig everywhere in the body

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35
Q

What are Peyer’s Patches?

A

Induction site for antigen-specific immune responses in the gut

36
Q

Where are Peyer’s Patches found?

A

In the gut - in the ileum

37
Q

How do Peyer’s Patches work?

A

No microvilli, so Ag is attracted. M cells take the Ag up by endo/phagocytosis, which then transport it to vesicles and release it at the basal surface. DCs meet the Ag at the basal surface and activate T cells!

38
Q

How are T cells homed to the gut?

A

They bind MAdCAM-1 on endothelium; epithelial cells express chemokines to attract them

39
Q

What is the mucosal lymphocyte life cycle?

A

B and T cells go through the bone marrow/thymus and circulate in the bloodstream. They then enter Peyer’s patches. If no Ag is encountered, they exit via lymphatics and renter the bloodstream. If Ag is encountered, cells are activated.

40
Q

What is a4b7?

A

Homing receptor triggered by GALT DC - binds to MAdCAM-1 expressed on gut endothelial cells

41
Q

What does CCR9 do?

A

Homing receptor triggered by GALT DC - binds to CCL25 on gut epithelium

42
Q

What is IgA?

A

Dominant immunoglobulin class in gut and respiratory tract; in blood it is mostly a monomer, but in mucosa it dimerizes (linked by J chain); class switching from IgM to IgA producing cells occurs in response to TGFb; binds and neutralizes antigen - does NOT trigger inflammation or complement

43
Q

What is oral tolerance?

A

The state of local and systemic immune unresponsive mess that is induced by oral administration of innocuous antigen such as food proteins

44
Q

What are the firewalls against commensalism bacteria?

A
  1. Sequestration in the lumen; 2. Quenching innate immune responses; 3. Penetrating commensalism induce bacterial clearance and pro inflammatory immune responses; 4. Commensalism bacteria are stopped in the mucosal lymph nodes
45
Q

How do neutralizing antibodies in vaccines prevent patient from getting sick?

A

Blocked attachment, blocked endocytosed, and blocked in coating

46
Q

What can a memory T cell produce?

A

IFNg, IL2, TNFa, IL4, IL5

47
Q

What are the different kinds of vaccines?

A
  1. Killed bacteria/inactivated viruses; 2. Live-attenuated viruses; 3. Subunit vaccines (toxin protein or surface viral protein); 4. DNA vaccines (NOT LICENSED IN HUMANS)
48
Q

How does virus attenuation work?

A

Virus isolated from human and then used to infect animal; that virus mutates to grow well in the animal and no longer grows well in human cells

49
Q

How do toxin subunit vaccines work?

A

Toxin binds to cell-surface receptor; endocytosis of the toxin:receptor complex; neutralizing antibody blocks binding of toxin to cell-surface receptor

50
Q

Define: adjuvant

A

Acts as a delivery system for vaccine; provides second signal and stimulates innate immunity while allowing antigen sparing

51
Q

What is alum?

A

Emulsion adjuvant that is most common in human vaccines; stimulates Th2 response and activates inflammasome

52
Q

What is MF59?

A

Squalene oil-in-water adjuvant emulsion; stimulates Th2

53
Q

What is MPLA?

A

TLR4 agonist, stimulates Th1 response, adjuvant

54
Q

What is the new big idea for flu vaccines?

A

Target the invariant HA stem structure to generate cross-reactive antibodies against all flu strains

55
Q

Why was the RSV vaccine discontinued?

A

Resulted in exacerbated pneumonia and lung pathology following RSV infection - increased eosinophilia infiltration due to pathological Th2-mediated response (hyper immune response)

56
Q

What is the new idea for RSV vaccine?

A

Monoclonal anti-F protein Ab given to infants at risk from RSV

57
Q

What B cell development is antigen independent? Dependent?

A

Independent: generation of B cells in the bone marrow; dependent: Ig class switch, somatic hyper mutation, germinal center reaction

58
Q

How many HC alleles are there? Light chain?

A

HC: 2; LC: 4

59
Q

What surface Ig is produced on immature B cells?

A

IgM

60
Q

Which occurs first - HC or LC rearrangement?

A

HC

61
Q

What is the process of heavy chain rearrangement?

A
  1. DJ on both alleles; V-DJ on one allele; 2. If productive, then preBCR is formed, HC rearrangement is stopped, LC rearrangement beings; 3. If non-productive, V-DJ on second allele; 4. If still not productive, cell death
62
Q

What are the two checkpoints for allelic exclusion in BCR formation?

A

Pre-B receptor; B receptor

63
Q

What is the difference between central tolerance and peripheral tolerance?

A

Central: established in lymphocytes developing in central lymphoid organs (clonally deletion); Peripheral: tolerance to self antigens established in lymphocytes in the peripheral tissues (clonal deletion, a nervy, clonal ignorance)

64
Q

What are the parts of antigen-independent b-cell development?

A
  1. DNA rearrangements (creating diversity); 2. Allelic exclusion (ensures that each clone expresses a single antibody on the surface - specificity); 3. Deletion of self-reactive clones (tolerance)
65
Q

Where does antigen-dependent B-cell development occurs?

A

Germinal center

66
Q

What are the processes of antigen-dependent b-cell development?

A
  1. T-cell dependent activation of antigen-specific naive B cells; 2. Somatic hyper mutation and IG class switch; 3. Differentiation of antigen-selected germinal center B cells into memory B cells and plasma cells
67
Q

What is somatic hyper mutation?

A

Random mutagenesis in V regions (mostly single base changes), associated with DNA strand breaks, supporting enzyme is activation-induced deaminase (AID)

68
Q

What is class switch recombination?

A

A DNA rearrangement that allows the same VDJ to be expressed with different heavy chain constant regions; uses AID enzyme

69
Q

What are the mechanisms for class switch?

A
  1. RNA processing: IgM to IgD; 2. DNA rearrangement: IgM to IgG, IgA, or IgE
70
Q

What occurs in the Dark Zone?

A
  1. Proliferation of B cells; 2. Generation of antibody-variants by SHM
71
Q

What occurs in the Light Zone?

A
  1. Selection (for high-affinity B cell clones and against self-reactive clones); 2. Generation of different antibody isotypes by class switching; 3. Differentiation into memory B cells and plasma cells
72
Q

What is a memory B cell?

A

No Ig secretion, but rapid response to renewed antigen encounter - circulates b/w lymphoid tissues through the blood

73
Q

What is a plasma cell?

A

Secretes Ig w/ high affinity; home to the bone marrow

74
Q

What is X-Linked Agammaglobulinemia?

A

Deficiency in tyrosine kinase; developmental arrest @ pre-B cell stage, so no circulating B cells, no IgM, IgG, IgA, or IgE

75
Q

What is Hyper-IgM Syndrome?

A

Deficiency of CD40L, CD40, or AID; abundant low-affinity serum IgM; no IgG, IgA, or IgE

76
Q

What can happen when there are chromosomal trans locations that affect B cells?

A

Sarcomas, leukemias, lymphomas

77
Q

Where do most B cell lymphomas originate?

A

germinal center B cells

78
Q

What do Rag-1 and -2 do?

A

They’re enzymes responsible for VDJ recombination

79
Q

What does chemo target?

A

Proliferating cells - causes a lot of collateral damage

80
Q

What does anti-tyrosinase do?

A

Targets melanoma but destroys melanocytes

81
Q

Explain Rituximab

A

Human-mouse monoclonal antibody; patient has no detectable B cells for 6-9 months, but IgG and IgA OK

82
Q

What is MUC-1?

A

Mucin normally expressed in lungs, GI tract, breast, reproductive tracts; marker of many cancers due to overexpression - dysregulation signifies more tumors problems

83
Q

What is MUC-16?

A

Better known as CA-125; used as blood bio marker for ovarian cancer to monitor for treatment response and for cancer recurrence

84
Q

How do glycolipids affect cancer?

A

Overexpressed on neuroblastoma, melanoma, sarcoma; targeted by vaccines and monoclonal antibodies

85
Q

What is BCR-ABL?

A

Gene that represents 9:22 translocation, known as the “Philadelphia Chromosome”; seen in chronic myelogenous leukemia

Immunology (6 decks)

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