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Pharmacology II > Immunopharmacology - Immune Diseases > Flashcards

Immunopharmacology - Immune Diseases Flashcards

1
Q

5 roles of the immune system? what are their implications?

A
  1. Defense against infections (vaccines)
  2. Defense against tumors (cancer)
  3. Clearance of dead cells and tissue repair (deficient:secondary infections, excessive:fibrosis/organ dysfunction)
  4. Injure cells and induce inflammation (allergic reactions/inflammatory diseases)
  5. Recognizes/responds to tissue grafts and new proteins (transplantations and gene therapy)
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2
Q

Two types of immunity? which one is always present? which one is more potent?

A

Innate : always present

Adaptive : more potent

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3
Q

Cells involved in innate immunity? (4)

A

Phagocytes
Dendritic cells
Complement
NK cells

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4
Q

Cells involved in adaptive immunity? (2)

A 
B lymphocytes
T lymphocytes (effector T cells)
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5
Q

3 types of cells of the immune system?

A

Lymphocytes
Antigen-presenting cells (APCs)
Effector cells

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6
Q

Role of lymphocytes?

A

Mediates adaptive immune response, only cells with specific receptors for antigens

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7
Q

Role of APCs? 4 cells?

A

capture, concentrate, display antigens for lymphocyte recognition
Dendritic cells, macrophages, B cells, follicular dendritic cells

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8
Q

Role of effector cells? 3 cells?

A

Eliminate microbes

Lymphocytes, Granulocytes, Macrophages

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9
Q

Which cells make antibodies?

A

B cells

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10
Q

How are B cells activated? (2)

A

Antigen must bind to sites

Stimulation by Helper T cells

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11
Q

3 types of T cells?

A

Helper T cells
Cytolytic T cells
T-regulatory cells (Tregs)

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12
Q

What do Helper T cells produce?

A

CD4, helps bind to class II MHC complexes on antigen presenting cells

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13
Q

What do Cytolytic T cells produce?

A

CD8 protein, binds transplanted tissue, infected cells, cancer cells

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14
Q

Role of Tregs?

A

Suppress activation of immune system to help maintain homeostasis

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15
Q

Development of B and T cells in Generative lymphoid organs (3) and Peripheral lymphoid organs?

A 
Generative lymphoid organs : 
-B lymphocyte and T lymphocyte lineage produced by bone marrow stem cell
-B transported to Bone marrow
-T transported to thymus
Peripheral:
-Mature B circulates in blood
-Mature T circulates in blood and lymph
-Both transported to Lymph nodes, Spleen and Mucosal and cutaneous lymphoid tissues
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16
Q

Two types of adaptive immunity?

A

Humoral

Cell-mediated

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17
Q

Humoral immunity:

Which lymphocyte acts on microbe? Overall function?

A

B lymphocyte

Blocks infections and eliminates extracellular microbes

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18
Q

Cell-mediated immunity:

Two lymphocytes? Which type of microbes do they each respond to and what is their function?

A

Helper T lymphocyte:
Responds to phagocytosed microbes in macrophages, activates macrophages and kills microbes

Cytotoxic T lymphocyte:
Responds to Intracellular microbes, kills infected cells and eliminates reservoirs of infection

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19
Q

4 steps of the immune response?

A
  1. Antigen recognition and presentation
  2. IL-1 production
  3. IL-2 and other cytokine expression
  4. Lymphocyte proliferation and differentiation
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20
Q

What are immunomodulators: two types of immunomodulators?

A

Agents that will modulate the immune system

Immunosuppressants and immunostimulant

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21
Q

3 immunostimulatory cytokines?

A

Interleukins
Colony stimulating factors
Interferon

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22
Q

2 types of colony stimulating factors? what are their roles?

A

G-CSF
GM-CSF
Stimulates division and proliferation of various stem cell types

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23
Q 
3 types of interferons? 
Which disease are they involved in?
Are they all:
viral or antiviral?
proliferative or antiproliferative?
Which one induces MHC II on top of MHC I?
A 
alpha (anticancer)
beta (relapsing MS)
gamma (chronic granulomatous disease)
-Antiviral
-Antiproliferative
-Gamma
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24
Q

2 other types of stimulants?

A

Thymic hormones

Adjuvants of bacterial origin

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25
Q

4 major classes of immunosuppressants?

A

Corticosteroids
Calcineurin inhibitors
Antiproliferative/Antimetabolic agents
Biologic (Ab)

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26
Q

3 examples of corticosteroids?

It decreases inflammation caused by what? (4)

A

Prednisone, Dexamethasone, Cortisol

Cytokines, NO, Prostaglandins, Leukotrienes

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27
Q

3 examples of NSAIDS?

A

Aspirin
Ibuprofen
Acetaminophen

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28
Q

3 drugs that reduce production of IL-2 from T cells

A

Cyclosporin A
Tacrolimus
Rapamycin

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29
Q

3 Anti-TNFa biologicals?

A

Infliximab
Etanercept
Adalimumab

30
Q

4 treatments of auto-immune disease?

A

Corticosteroids
NSAIDS
Drugs that reduce IL-2 production
Anti-TNFa biologicals

31
Q

Difference in potency between dexamethasone vs. prednisone and cortisol?

A

20-30x more potent that cortisol

4-5x more potent than prednisone

32
Q

MOA of corticosteroids? (2)

A

Transactivation : activates expression of anti-inflammatory genes
Transrepression : decreases expression of pro-inflammatory genes

33
Q

MOA of tacromilus?

A

binds to FK506-binding protein
forms FK506-FKBP complex
binds to and blocks CaN
FK506-FKBP-CaN complex inhibits activation of NF-ATc, preventing entrance into nucleus

34
Q

MOA of cyclosporin?

A

CsA binds to immunophilin, cyclophylin (CpN
CsA-CpN binds to and blocks CaN function
Failure of CaN to dephosphorylate NF-ATc, inhibiting it’s transport into the nucleus

35
Q

Anti-TNFa biologicals only bind human TNF-a with high…? (3)

A

Specificity
Affinity
Avidity

36
Q

What is the main disease treated by immunosuppressants? What are two general mechanisms of this disease?

A

Autoimmune diseases

  1. Failure of auto-antibodies and T cells to recognize own cells
  2. Auto-antibodies and T cells launch attack against own cells
37
Q

3 ways autoimmune diseases can develop?

A
  1. Spontaneous
  2. MHC associated genetic predispositions
  3. Infectious agents
38
Q

MOA of autoimmune disease induction? (6)

A
  1. Infectious agent causes disease
  2. Recovery from disease (T cell and Ab response)
  3. A portion of a protein from infectious agents mimics a self protein
  4. Due to MHC composition, some T cells specific for infectious agent protein also cross-react with self protein
  5. T cell becomes pathogenic, responds to self antigen, recruits other immune cells
  6. Tissue destruction
39
Q

How is the classification of autoimmune diseases separated? Three classes?

A

Effector mechanism

Type II, Type III, Type IV

40
Q

Type II autoimmune disease is a _______ mediated disease

A

antibody

41
Q

Example of a type II autoimmune disease?

A

Graves disease

42
Q

Graves disease happens in the ______ and it makes antibodies for which receptor? This leads to what disorder?
These antibodies act as _____

A

Thyroid
Thyroid-stimulating hormone receptor (TSHR)
Hyperthyroidism
Agonists

43
Q

Is it possible to transmit Graves Disease to fetus?

How can this be cured

A

Yes, antibodies can cross the placenta

Plasmapheresis removes maternal anti-TSHR Abs and cures the disease

44
Q

Type III autoimmune diseases are ______-_____ diseases

A

Immune-complex

45
Q

4 processes that immune complexes can be subject to?

A

Complement deposition
Opsonization
Phagocytosis
Processing by proteases

46
Q

Immune complexes in which autoimmune diseases? (5)

A 
Lupus erythematosus
Cryoglobulinemia
Rheumatoid Arthritis
Scleroderma
Sjogren's syndrome
47
Q

Type IV autoimmune diseases are mediated by which cells?

A

T cells

48
Q

4 examples of Type IV autoimmune diseases?

A

Diabetes mellitus
Rheumatoid arthritis
MS
Celiac disease

49
Q

Antigen and consequence of Insulin-dependent diabetes mellitus?

A

Pancreatic Beta-cell antigen

Beta-cell destruction

50
Q

Antigen and consequence of Rheumatoid Arthritis?

A

Unknown synovial joint antigen

Joint inflammation and destruction

51
Q

Antigens (2) and consequences (2) of MS?

A

Myelin basic protein, proteolipid protein

Brain degeneration, paralysis

52
Q

Antigen and consequences (2) of Celiac disease?

A

Gluten modified by tissue transglutaminase
Malabsorption of nutrients
Atrophy of intestinal villi

53
Q

4 T-cell mediated effects in type IV autoimmune diseases?

A
  1. T cell cytotoxicity via CD8+ cytotoxic T lymphocytes
  2. Self-destruction of tissue cells induced cytokines
  3. Recruitment and activation of macrophages leading to bystander tissue destruction
  4. Induction of target tissue apoptosis by the T cell membrane protein FasL
54
Q

In rheumatoid arthritis, _____antigens cause non-specific activation of T-cells resulting in what? (2)

A

Superantigens
Polyclonal T cell activation
Massive cytokine release

55
Q

In rheumatoid arthritis, the immune complex precipitates on synovial lining, what is the MOA? (6)

A
  1. Complement deposits
  2. Macrophages infiltrate synovium and become activated
  3. CD4 and CD8 lymphocytes infiltrate synovium
  4. Th1 cytokine secretion predominates
  5. Infiltration of B cells
  6. Acute inflammation occurs with destruction of cartilage and bone
56
Q

Psoriasis is a Type IV autoimmune disease that causes activation of T cells where?

A

in skin cells

57
Q

Topical medications of psoriasis? (7)

A 
Corticosteroids
Vitamin D analogue creams
Topical retinoids
Moisturizers
Topical immunosuppressants
Coal tar
Anthralin
58
Q

Example of a vitamin D analogue to treat psoriasis?
It acts mainly on which receptor?
Vitamin D3 inhibits production of ___ and ____
Blocks transcription of ______ and _______
Inhibits activity of which cells? (2)

A 
Calcipotriene (Dovonex)
Vitamin D receptor (VDR)
IL-2 and IL-6
IFN-gamma and GM-CSF
Cytotoxic T cells and natural killer cells
59
Q

Vitamin D3 inhibits proliferation of which cells?

A

Keratinocytes

60
Q

Which biological agent interferes with lymphocyte activation?

A

Alefacept

61
Q

Which biological agent blocks TNFa and TNFB binding to receptor?

A

Etanercept

62
Q

Which two biological agents and monoclonal antibodies that block TNFa binding to receptor?

A

Infliximab

Adalimumab

63
Q

Three types of organ donors? Explain

A

Syngeneic : between genetically identical individuals
Allogeneic : from one individual to another of the same species
Xenogeneic : between individuals of different species

64
Q

3 Types of Host vs. Graft organ rejection?

A

Hyperacute
Acute
Chronic

65
Q

Onset of hyperacute organ rejection?

Mechanism?

A

Immediate
Abs against donor tissue, caused by accidental ABO blood type incompatibility.
Presents while still in surgery with thrombosis and occlusion of graft vessels

66
Q

Onset of acute organ rejection? Mechanism?

A

Weeks to months
T-Cell mediated response against foreign MHC.
Inflammation and Leukocyte infiltration of graft vessels

67
Q

Onset of chronic organ rejection? Mechanism?

A

Months to years
T-cell mediated process from foreign MHC looking like self-MHC carrying an antigen.
Results in intimal thickening and fibrosis of graft vessels

68
Q

Mechanism of “Graft vs. Host” organ rejection?

A

Donor T-cells in graft proliferate and attack recipient’s tissue.
Commonly in bone marrow transplants. Presents with diarrhea, rash and jaundice

69
Q

Prior to transplants, patients receive which immunosuppressive regimen? (4)

A

Antithymocyte Globulin, Muromonab-CD3, Daclizumab or Basiliximab

70
Q

Muromonab-CD3 blocks what?

A

blocks killing by cytotoxic human T cells

71
Q

Basiliximab is what type of immunoglobulin? Role?

Similar drug? Where does this one bind?

A

IgG1
Binds to CD25, the IL-2 receptor alpha chain on lymphocytes
-IL-2 antagonist, blocks IL-2 from binding to lymphocytes
Daclizumab : binds to alpha subunit of IL-2

Pharmacology II (21 decks)

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