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PHAR 303 (toxicology) > Immunotoxicology > Flashcards

Immunotoxicology Flashcards

final exam

1
Q

role of neutrophil

A

bacterial, phagocytosis, inflammation

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2
Q

role of basophil

A

allergy, helminth infection

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3
Q

role of mast cell

A

allergy, parasitic infection

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4
Q

role of eosinophil

A

allergy, parasitic infection

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5
Q

role of macrophage

A

bacterial, phagocytosis, inflammation

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6
Q

role of dendritic cell

A

present antigen for immune response; bridge the gap between innate and adaptive immunity

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7
Q

role of b cells

A

antibody production; neutralize pathogens, allergy

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8
Q

role of t cells

A

protect from pathogens, destroy infected cells, produce CD4+ and CD8+ t cells

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9
Q

role of natural killer cells

A

tumors, infected cells

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10
Q

immunotoxicology

A

any adverse effect on the structure or function of the immune system, or on other systems as a result of immune system dysfunction

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11
Q

problems that can occur due to immunotoxicology

A
  • immunosuppression: Impaired immunity → Enhanced susceptibility to infection
  • immunoenhancement: Autoimmunity, Hypersensitivity, Chronic inflammation
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12
Q

what is azathioprine used for?

A

immunosuppressive agent used to treat diseases such as rheumatoid arthritis and IBD

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13
Q

mechanism/effect of azathioprine

A
  • pro-drug converted to active metabolite, 6-mercaptopurine (in liver)
  • XO and TPMT convert it to an inactive metabolite that is cleared from the body
  • active metabolite is structurally similar to purine bases, so incorporated into DNA and RNA, which causes:
  • Strand breaks, inhibition of DNA
    repair, inhibition of replication
  • Inhibition of B and T cell proliferation
  • Induces apoptosis
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14
Q

adverse effect of azathioprine and what causes this adverse effect (mechanism)

A

Dose-dependent adverse effect caused by elevated concentrations of 6-TGNs – myelotoxicity
- 6-mercaptopurine is converted to 6-TGN by HPRT and GMP synthase, which can cause life-threatening pancytopenia (when too much)
- elevated 6-TGN can be due to and inherited TPMT deficiency (less inactivation of 6-MP)
- or when with allopurinol, which inhibits XO

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15
Q

what is clozapine used for?

A

anti-psychotic medication for schizophrenia when other meds don’t work

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16
Q

mechanism/effect of clozapine side effect

A

this occurs in a dose-independent manner (don’t know why this occurs):
- converted to nitrenium ion by MPO, which is highly expressed in neutrophils
- ion leads to GSH and ATP depletion, which leads to oxidative stress
- this leads to apoptosis and neutropenia (aka neutrophil depletion)

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17
Q

effect of tobacco smoke

A
  • have both immunosuppressive and immunoenhancing effects
  • causes lung inflammation by increasing the recruitment of innate cells, which then release more mediators (Th1/Th17/CD8+ T cells)
  • also reduces macrophage ability to phagocytose and/or kill bacteria, making them more susceptible to respiratory infection
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18
Q

effect/mechanism of cannabis

A
  • THCA (inactive) converted to THC (active) by heat
  • binds to CB1 (in CNS) and CB2 (immune cells) receptors
    immunosuppression
  • induces apoptosis, inhibits proliferation, suppresses pro-inflammatory cytokines (TNF-a, IFN-y, IL-2), and induces T regulatory cells
  • this causes, T cell response to shut down and suppresses autoreactive T cells
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19
Q

which immune cells have the most to least CB2 receptors (at the mRNA level)?

A
  1. B cells
  2. NK cells
  3. macrophages
  4. monocytes
  5. PMN
  6. T cell
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20
Q

what are some chemicals in the halogenated aromatic hydrocarbon family? which is the most toxic?

A
  • dioxin (TCDD) – most toxic
  • PCDFs
  • PCBs
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21
Q

dioxin acts through which pathway?

A

AhR pathway

22
Q

role of thymus

A
  • primary lymphoid organ
  • site of T-cell maturation (immature T-cell migrate from bone marrow)
23
Q

growth of thymus organ (what is max size, when doe sit reach that size, what happens afterwards)

A
  • reaches max size at puberty
  • 30-40g
  • declines after
24
Q

effect of dioxin in cellular models

A

indices thymic atrophy (decreases size and cellularity)

25
Q

effect of dioxin in humans

A

decrease in IgG levels, causes chloracne acutely

26
Q

autoimmunity definition

A

When the immune system mistakenly recognizes self-tissue as foreign- and then attack – loss of self-tolerance

27
Q

main effects of autoimmunity

A

chronic inflammation and tissue damage

28
Q

what is self-tolerance

A

lack of immune response to one’s own tissue antigens

29
Q

how is loss of self-tolerance achieved? what is the result?

A
  • Autoreactive lymphocytes escape elimination by central tolerance mechanisms, these then go to periphery where they encounter specific autoantigens
  • Peripheral tolerance mechanisms (secondary lymphoid organs and/or sites of inflammation) also fail in stopping activation of autoreactive lymphocytes, this leads to specific response against autoantigen-bearing cells, leading to tissue damage.
30
Q

mechanism of normal immunologic tolerance

A
  • central: deletion, development of regulatory T cells, receptor editing (for B-cells)
  • peripheral: anergy (b-cells), apoptosis by self-antigen recognition, and suppression of t regulatory cells
31
Q

what is anergy?

A

functional inactivation because co-stimulatory molecule on APC is not delivered

32
Q

clinical symptoms/mechanisms of autoimmune diseases

A

Activated T cells release proinflammatory cytokines:
- Activate innate immune cells (such as macrophages and neutrophils) as well as nonhematopoietic cells (such as endothelial cells and fibroblasts) to induce the production of more cytokines
- Autoreactive CD4+ cells, or helper T (Th) cells, also help autoreactive B cells in autoantibody production
- Th cells can also activate autoreactive CD8+ cytotoxic T (Tc) cells
inflammation and damage

33
Q

postulated mechanism of autoimmunity

A
  • genetic: by influencing the maintenance of self-tolerance
  • environment (e.g. tobacco, drugs, UV, solvents, heavy metals): causes tissue damage/inflammation that cause activation of self-reactive lymphocytes through:
    • cell death making hidden material available to APCs
      - formation of neoantigens from covalent binding of chemicals to tissue
  • hormones: some are more common in women
34
Q

what factors can lead to systemic lupus erythematosus?

A

genetic and environmental (most is idiopathic – due to drugs) – cigarette smoke, silica, etc.

35
Q

where and how is damage caused in lupus?

A

Can involve any organ in the body but usually affects skin, kidneys, joints and heart – damage by immune complex deposition (pathogenesis not well understood)

36
Q

which drugs can cause drug-induced lupus?

A

isoniazid and hydralazine hydrochloride

37
Q

most common clinical presentation of lupus

A

skin-rash

38
Q

treatment of drug-induced lupus

A

discontinuation of offending drug

39
Q

what is systemic sclerosis (and where does it usually occur)

A

Autoimmune disease of connective tissue, characterized by fibrosis (usually localized – skin of hands, feet, face)

40
Q

who is more susceptible to systemic sclerosis?

A
  • women more affected
  • occurs middle-age
41
Q

risk factors of systemic sclerosis

A

chemicals – vinyl chloride

42
Q

where is vinyl chloride used?

A

used to make PVC plastics

43
Q

main exposure route of vinyl chloride

A

inhalation (workers)

44
Q

effect of vinyl chloride

A

leads to an abnormal protein that is antigenic – systemic sclerosis

45
Q

hypersensitivity reaction definition and common feature

A
  • over-reaction of the immune system
  • prior exposure leading to sensitization to elicit reaction upon subsequent challenge
46
Q

types of hypersensitivity reactions

A

– Type I (Immediate hypersensitivity)
– Type II (Antibody-mediated)
– Type III (Immune-complex mediated)
– Type IV (T-cell mediated)

47
Q

type I hypersensitivity reaction mechanism

A

sensitization (1st exposure)
1. allergen enters mucosa and is picked up by dendritic cells
2. dendritic cell primes T cell in lymph nodes
3. plasma cell travels back to mucosa and produces allergen-specific IgE antibodies
re-exposure:
4. allergen-specific IgE binds to mast cell and triggers mast cell degranulation
5. leads to asthma, anaphylaxis (allergy)

48
Q

occupational asthma due to high or low molecular weight agents?

A

low

49
Q

use of toluene diisocyanate (TDI)

A

produce polyurethanes (adhesives, pillows, mattresses, sealants)

50
Q

exposure of toluene diisocyanate (TDI)

A
  • Cured TDI (foam) is inert and non-toxic
  • so by occupational exposure (inhalation)
51
Q

predicted mechanism for TDI-induced asthma

A
  1. it damages lung epithelial cells
  2. GSH exhausted so leads to oxidative stress
  3. forms neoantigens from airway proteins and recognition as non-self
  4. in some people, this can lead to Th2 response hypersensitivity reaction (type 1)

PHAR 303 (toxicology) (14 decks)

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