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Pharmaceutics > Immunology > Flashcards

Immunology Flashcards

1
Q

Components of Innate Immunity:

5

A
  1. physical and chemical barriers
  2. inflammation
  3. fever
  4. cells
  5. chemicals
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2
Q

antimicrobial peptides (AMPs), key points (4)

A
  1. mostly short peptides
  2. broad spectrum, less specific (target gram positive, gram negative, fungi)
  3. kill microbes
  4. interact with adaptive immune system (recruit T cells…)
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3
Q

AMP examples (4)

A
  1. Cathelicidins (LL-37)
  2. Defensins
  3. Lysozyme
  4. RNase 7
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4
Q

Defensins, key points (3)

A
  1. short, disulfide-rich peptides
  2. amphipathic (accumulate in cell membranes, form and defend pores)
  3. induced by presence of pathogen on a surface
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5
Q

General diseases associated with AMPs

A

up or down-regulation of AMPs associated with inflammatory skin and inflammatory bowel diseases

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6
Q

Bacterial Lipopolysaccharide

A

virulence factor, initiator of inflammation, target of innate immune system

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7
Q

Complement System, key points (3)

A
  1. biosynthesized in the liver
  2. ~20 soluble proteins circulating in blood and extracellular fluid
  3. mostly inactive precursors, activated by proteolytic cascade
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8
Q

Classical Pathway

A
  1. C1 binds IgG/IgM (part of acquired immunity)
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9
Q

Alternative Pathway

A
  1. C3 binds microbial lipopolysaccharide
  2. direct lysis of pathogens
  3. induce inflammation
  4. promote phagocytosis
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10
Q

Mannose Binding

A
  1. Mannan-binding lectin (MBL) binds microbial mannose
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11
Q

Complement System, components

A
  • C1 binds IgM/IgG (classical pathway activation)
    • C3 binds microbial lipopolysaccharide (alternative pathway activation)
    • C3 products can contribute to B cell activation
    • C3b is a strong opsonization signal
    • C5a is a potent chemotactic factor
    • C3a, C4a and C5a contract smooth muscle and increase vascular permeability (this produces local swelling and “walls off” sites of infection. These factors also participate in anaphylactic reactions)
    • C5,6,7,8 and 9n create membrane attack complex that can lyse targeted cells by breaking their cell walls
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12
Q

Pattern Recognition Receptors (PRRs)

A

recognize pathogen-associated molecular patterns (PAMPs): unique, vital, conserved products of pathogens;
stimulate chemical defenses (interferons, AMPs…), inflammation, cytokines, adaptive immune system…

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13
Q

Toll-Like Receptors (TLRs)

A

intra and extracellular pattern recognition receptors, ‘alarm system’ for both innate and adaptive immune systems

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14
Q

NOD-Like Receptors (NLRs)

A

intracellular pattern recognition receptors

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15
Q

Inflammation is…

A

a localized protective response to tissue damage (injury, infection, irritation, allergy)

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16
Q

Inflammation, key points

A

Coordinated, multi-stage response by cellular and non-cellular components

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17
Q

Stages of Inflammation (5)

A
  1. clotting, complement (platelets release clotting factors)
  2. mast cells degranulate, vasodilation, WBC migration (mast cells release factors (vasodilation, vasoconstriction, permeability–deliver troops))
  3. neutrophils degranulate (neutrophils release factors to kill pathogens)
  4. neutrophils and macrophages phagocytose pathogens
  5. macrophages release cytokines to recruit immune cells and tissue repair
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18
Q

Symptoms of Inflammation (4+1)

A
  1. rubor (blood flow)
  2. calor (blood flow)
  3. tumor (exudate)
  4. dolor (exudate, bradykinin)
  5. loss of function
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19
Q

Functions of Inflammation (3)

A
  1. confine pathogens
  2. destroy pathogens
  3. repair tissue
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20
Q

Inflammation can progress from acute to chronic to granuloma formation (wall off site)

A

:(

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21
Q

Kinin system

A

in long-term inflammation, cause endothelial cell retraction to increase vascular permeability

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22
Q

Functions of Complement System (5)

A
  1. opsonization (C3b)
  2. chemotaxis (C5a)
  3. anaphylatoxins (C3a, C4a, C5a)
  4. cytotoxins (C5,6,7,8,9n form membrane attack complex)
  5. initiate inflammation
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23
Q

Clotting system activated by:

A

collagen, proteases, kinins, bacterial endotoxins

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24
Q

Clotting system is balanced by:

A

fibrinolysis (plasminogen being converted to plasmin)

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25
Q

Kinin system, cascade and effects (5)

A

activated by first step in clotting cascade, ultimately produces bradykinin, which:

  1. vasodilation
  2. smooth muscle contraction
  3. vascular permeability
  4. WBC chemotaxis
  5. pain
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26
Q

Mast cell component of cellular response

A

mast cells release histamine, neutrophil and eosinophil chemotactic factors, and leukotrienes (smooth muscle contraction, increase vascular permeability), prostaglandins, cytokines;
important in trauma

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27
Q

Resident macrophages component of cellular response

A

phagocytosis;

toll-like receptor activation, release TNF-a and IL-1, important in chronic inflammation

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28
Q

Exudate

A

any fluid that filters from circulatory system into lesions/areas of inflammation

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29
Q

Exudate functions (3)

A
  1. dilutes toxins (from bacteria and dying cells)
  2. carries away toxins, dead cells, inflammatory products
  3. brings in plasma proteins (antibodies, leukocytes)
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30
Q

Types of Exudate (3)

A
  1. early (watery)
  2. severe inflammation (pus, leukocytes)
  3. hemorrhagic (bleeding, erythrocytes)
31
Q

WBC migration into tissue

A

coordinated response: need signal to activate both WBC and endothelial cell

32
Q

important WBCs from acute to chronic inflammation (4)

A 
(acute inflammation)
1. neutrophils
2. eosinophils
3. macrophages
4. T-cells
(chronic inflammation)
33
Q

platelets component of cellular response

A

activated by damaged tissue, release histamine and serotonin, aggregation

34
Q

neutrophils component of cellular response

A

activated by invaders or mast cells, phagocytosis, secrete factors to kill pathogens

35
Q

Margination

A

movement from blood into tissue

36
Q

oxygen dependent killing

A

phagocytes generate toxic oxygen-containing molecules and radicals

37
Q

Types of Lesions (5)

A
  1. granulomas (TB, leprosy, syphilis)
  2. fibrinous inflammation (vascular permeability allowing fibrin to pass through; cancer)
  3. purulent inflammation (pyogenic bacteria)
  4. serous inflammation (copious effusion of serous fluid; skin blisters)
  5. ulcerative (necrotic loss of tissue from the surface exposing lower layers; ulcer)
38
Q

Resolution (5)

A
  1. Termination of inflammation
  2. Regeneration (proliferation of cells)
  3. Resolution (restoration of normal tissue structure and function)
  4. Repair (scar tissue replaces damaged tissue)
  5. Maturation (wound contraction, remodeling of scar tissue)
39
Q

Chronic Inflammation

A

Duration of two weeks or longer

40
Q

Antibody Effects:

A
  1. opsonization
  2. complement activation (IgG/IgM C3)
  3. neutralization, agglutination, precipitation
41
Q

What are antibodies?

A

glycoproteins that specifically bind target antigens

42
Q

What is an antigen?

A

molecules that induce an immune response

43
Q

Fab

A

fragment of antibody including heavy and light chain with variable regions

44
Q

Fc

A

fragment of antibody including just heavy chain constant region

45
Q

The hypervariable loop of an antibody is the complementarity determining region

A

:)

46
Q

Why is glycosylation of antibodies important?

A

affects pharmacokinetic profile (half-life)

47
Q

How do we generate more unique antibodies than genes in our genome, short answer?

A

somatic recombination

48
Q

How do we generate light chain diversity?

A

VJ somatic recombination:
short repetitive sequences (germ line DNA) –> rearranged B lymphocyte DNA –> transcription (primary transcript) –> alternative mRNA splicing (immunoglobulin mRNA)

end with one V (variable) and one J (joining) region

49
Q

How do we generate heavy chain diversity?

A

VDJ somatic recombination

50
Q

RAG protein

A

responsible for cutting and splicing performed in somatic recombination; recognizes specific sequences

51
Q

purpose of somatic hypermutation

A

improve antibody affinity on subsequent encounters; activation-induced deaminase (AID) purposefully introduces mutation

52
Q

How do we increase antibody diversity? (4)

A
  1. V(D)J recombination of heavy chain and light chain
  2. diversity due to heavy and light chain joining
  3. junctional diversity (imperfect joining of V and J/D segments)
  4. somatic mutations
53
Q

Encounter with self-antigen results in:

A

clonal deletion/apoptosis (multivalent self-antigen) or anergy/unresponsiveness (soluble self-antigen)

54
Q

Receptors/surface proteins on antigen-presenting cells (2)

A
  1. MHC-II

2. B7

55
Q

Receptors/surface proteins on mature B cells (3)

A
  1. IgM
  2. IgD
  3. MHC-II
56
Q

Receptors/surface proteins on helper T cells

A

with APC:

  1. TCR (with MHC-II of APC)
  2. CD4+ co-receptor (with MHC-II of APC)
  3. CD28 co-receptor (with B7 of APC)

with B cell:

57
Q

T cells release IL to activate B cells after they match

A

:)

58
Q

main players in humoral and cell-mediated immunity

A

humoral: B cells/plasma cells

cell-mediated: T cells/CTLs

59
Q

A few functions of T cells:

A
  1. cytokines to activate macrophages
  2. IL to activate B cells
  3. able to detect pathogens hiding in a host cell (unlike antibodies)
60
Q

T cell positive vs. negative selection

A

positive: must react to self MHC carrying peptides (otherwise apoptosis)
negative: do not react strongly to self-antigens on MHC
(2-5%)

61
Q

T cells defined by:

A

development in thymus, T cell receptors (TCR), specific MHC

62
Q

cytotoxic T lymphocytes (CTL)

A

CD8+ co-receptor

recognize MHC-I (infected self cell)

63
Q

helper T cells

A

TH1: inflammatory (activate macrophages, CTLs)
TH2: helper (activate B cells)

CD4+ co-receptor recognizes MHC-II (antigen presentation)
CD28 receptor with B7 of APC

64
Q

T cell receptor vs. B cell receptor

A

T cell receptor: univalent, similar to single Fab fragment

B cell receptor: bivalent, surface immunoglobulin (IgG/IgM)

65
Q

T cell receptor (TCR)

A

univalent
similar to single Fab fragment (alpha and beta chain)

unlike immunoglobulins, TCRs have no secreted form and do not recognize free antigens (must be presented on MHC)

66
Q

MHC-I

A

self

67
Q

MHC-II

A

antigen

antigen presenting cells

68
Q

MHC-I vs MHC-II differences in presenting peptide length

A

MHC-I: shorter (8-10 aa) peptides

MHC-II: longer (13+ aa) peptides

69
Q

MHC - T cell interactions

A

MHC interacts with TCR and CD8+/CD4+ co-receptor

70
Q

antigen presenting cells (APC)

A
  1. dendritic cells (MHC-I, MHC-II, B7)
  2. macrophages (PRR –> MHC-II, B7)
  3. B cells (MHC-II, CD40?)
71
Q

CD4+ T cell activation

A
  1. TCR/CD4+ interacts with MHC-II/antigen
  2. CD28 interacts with B7
  3. T cell stimulated by its own IL-2
72
Q

Cyclosporin

A

inhibits IL-2, preventing CD4+ T cell activation, resulting in immunosuppression and preventing rejection of transplant organs

73
Q

CD8+ T cell activation

A
  1. TCR/CD8+ interacts with MHC-I/antigen
  2. CD28 interacts with B7
  3. T cell stimulated by its own IL-2
74
Q

CTL killing mechanisms (2)

A
  1. perforins (form channels)

2. granzymes (signal apoptosis)

Pharmaceutics (4 decks)

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