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Immunology > Moudule 1 & 2 > Flashcards

Moudule 1 & 2 Flashcards

1
Q

The initial response by the immune system is determined by:

A
  1. the nature of the pathogen
  2. The environment in which the pathogen is encountered
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2
Q

Germ-line encoded receptors are:

A

PRRs (Found on innate cells)

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3
Q

Randomly generated receptors are:

A

BCRs and TCRs (found on adaptive cells)

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4
Q

Humoral immunity

A

Combats pathogens via antibodies (Abs)

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5
Q

Cell-Mediated immunity primarily involves:

A

T cells

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6
Q

Explain Clonal selection:

A

Is the process by which individual T and B lymphocytes are selected and cloned to create a large population (an army) of antigen-reactive cells that are identical.

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7
Q

Primary Response:

A

Initiated upon first exposure to an antigen.

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8
Q

Secondary response:

A

Initiated upon second exposure to the same antigen that stimulates memory lymphocytes.

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9
Q

Common Myeloid Progenitors

A
  1. Erythrocytes
  2. Granulocytes
  3. Monocytes/Macrophages
  4. Megakaryocytes
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10
Q

Common Lymphoid Progenitors (CLPs):

A
  1. B lymphocytes
  2. T lymphocytes
  3. Innate Lymphoid Cells (NK Cells)
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11
Q

CD:

A

Cluster of differentiation

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12
Q

CD4 and CD8 are:

A

Membrane glycoproteins on the surface of T cells

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13
Q

CD4 is expressed on

A

T helper (TH) cell

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14
Q

CD8 is expressed on:

A

T cytotoxic (Tc) cell

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15
Q

T helper subsets:

A

Th1, Th2, Th17, Treg, and Tfh

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16
Q

Primary Lymphoid Organs:

A

Bone marrow and Thymus

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17
Q

Secondary lymphoid organs are where lymphocytes:

A
  1. Encounter antigens
  2. Become activated
  3. Undergo clonal expansion
  4. Differentiate into effector cells
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18
Q

Secondary Lymphoid Organs:

A
  1. Draining Lymph nodes
  2. Spleen
  3. Mucosal-associated lymph tissues (MALT)
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19
Q

The 4 types of mucosal/epithelial lymphoid tissues:

A
  1. GALT (Gut)
  2. BALT (Bronchi)
  3. NALT (Nasal)
  4. SALT (Skin)
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20
Q

Signal transduction:

A

The binding interaction between a receptor and cognate ligand resulting in an intracellular molecular signaling pathway ending with an appropriate cellular response.

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21
Q

Cognate

A

Refers to 2 bio molecules that typically interact.

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22
Q

Ligand-receptor binding induces molecular changes in the receptor:

A
  1. Conformational change
  2. Dimerization/cluster
  3. Location on membrane will change
  4. Covalent modification (phospholation)
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23
Q

Receptors alterations induce cascades of intracellular events:

A
  1. Gene expression (start producing genes)
  2. Activate enzymes (ex: Actin —> needed fro phagocytosis.
    3.Intracellular location (will recruit proteins to its location)
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24
Q

The five distinct antibody isotypes:

A
  1. IgA: alpha
  2. IgD: delta
  3. IgE: epsilon
  4. IgG: gamma
  5. IgM: mu
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25
Q

ITAM:

A

Immunoreceptor tyrosine-based activation motif

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26
Q

Cytokines:

A

Proteins that communicate among cells of the immune system.

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27
Q

Endocrine:

A

Signaling molecules — synthesized and secreted by signaling cells.

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28
Q

Paracrine:

A

Signaling molecules affect only nearby receptor-expressing target cells.

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29
Q

Autocrine:

A

Cells respond to signals they secrete.

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30
Q

Pleiotropic:

A

Activity induces different biological effects dependent on target cell.

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31
Q

Redundant:

A

Activity mediates similar effects on target cell.

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32
Q

Synergy:

A

Effect combines two cytokines activities to be greater than additive effect.

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33
Q

Antagonistic:

A

Effect inhibits one cytokine’s effect by another’s action.

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34
Q

Cascade effect:

A

Effect of one cytokine on one target cell to produce additional cytokine(s).

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35
Q

Interleukin (IL-1):

A
  • Pro inflammatory (local inflammation), induces fever.
  • Simulates production of neutrophils.
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36
Q

IL-2:

A

Lymphocyte (T & B cells) proliferation

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37
Q

IL-4:

A

Th2 cell differentiation.
IgE class switching.
Anti-parasitic.
Allergies

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38
Q

IL-5:

A

Eosinophil production.
Anti-parasitic.
Allergies.

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39
Q

IL-6:

A

Pro-inflammatory.
Induces inflammation.
Fever.

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40
Q

IL-12:

A

Th1 cell differentiation.
IFN-gamma production.
Enhances CTL activity.

41
Q

Innate immune system includes:

A
  1. Anatomical barriers - both physical & chemical.
  2. Cellular responses.
42
Q

Anatomical Barriers: Physical

A

Skin and mucosal membranes

43
Q

Anatomical Barriers: Chemical

A

Acidic pH.
Enzymes and binding proteins.
Antimicrobial peptides.

44
Q

Families of cellular PRRs include:

A
  1. Toll-like receptors (TLRs)
  2. C-type lectin receptors (CLRs)
  3. NOD-like receptors (NLRs)
  4. AIM2-like receptors (ALRs)
  5. RIG-I-like receptors (RLRs)
45
Q

TLR PAMP (Ligand):

A

Extracellular pathogens, endocytosed, and phagocytosed.

46
Q

TLR Cellular Location:

A

Plasma membrane, endosomal membrane, lysosomal membrane.

47
Q

TLR Protective Response:

A
  • cytokines/chemokines get turn on.
  • pro inflammatory cytokines.
  • turn on type I IFNs (anti-virals).
  • turn on antimicrobial peptides.
48
Q

CLR PAMP (Ligand):

A

Fungal pathogens

49
Q

CLR Cellular location:

A

Plasma membrane

50
Q

CLR Protective Response:

A
  • cytokines/chemokines get turn on.
  • pro inflammatory cytokines.
  • turn on antimicrobial peptides.
51
Q

NLR PAMP (Ligand):

A

Intracellular/extracellular bacteria.
Bacterial cell wall components.

52
Q

NLR Cellular Location:

53
Q

NLR Protective Response:

A
  • cytokines/chemokines get turn on.
  • pro inflammatory cytokines.
  • turn on antimicrobial peptides.
  • induce inflammasome—> pyroptosis
54
Q

ALR PAMP (Ligand):

A

Viral and bacterial DNAs

55
Q

ALR Cellular Location:

56
Q

ALR Protective response:

A
  • cytokines/chemokines get turn on.
  • pro inflammatory cytokines.
  • turn on type I IFNs (anti-virals).
  • turn on antimicrobial peptides.
  • induce inflammasome—-> pyroptosis
57
Q

RLR PAMP (Ligand):

58
Q

RLR Cellular Location

59
Q

RLR Protective Response:

A
  • cytokines/chemokines get turn on.
  • pro inflammatory cytokines.
  • turn on type I IFNs (anti-virals).
60
Q

Innate immunity cellular responses: (4)

A

Inflammatory mediators
Phagocytosis
Programmed Cell Death
Inflammation
ILCs (NK cells)

61
Q

Pro-inflammatory cytokines do:

A
  • induce fever.
  • cause vascular permeability increase (more blood to get to tissues).
  • recruit leukocytes and activate them.
  • induce myeloid cell production.
62
Q

Enzymes that help generate antimicrobial and pro inflammatory mediators.

A

iNos and COX2

63
Q

iNOS

A

Induces nitric oxide synthase

64
Q

COX2 (cyclooeygenase-2):

A

coverts lipids to prostaglandins

65
Q

Apoptosis

A

Induced by TNF binding to the TNFR, NK cells, and cytotoxic T cells (CTLs).

66
Q

NETosis or Neutrophil extracellular traps (NETs): Activation requires…

A

Activation requires NADPH oxidase and generation of ROS.

67
Q

Pyroptosis:

A

Induced by inflammasome activation, eliminates infected macrophages allowing release of IL-1beta and IL-18. (& induce fever, increase myeloid production).

68
Q

Cardinal Signs of inflammation:

A
  1. Heat- Calor
  2. Redness - Rubor
  3. Swelling - Tumor
  4. Pain - Dolor
  5. Loss of function - Funtio laesa
69
Q

Activated NK cells perform one of the two functions:

A
  1. Kill the altered self-cell by releasing proteins that induce apoptosis.
  2. Produce cytokines that induce adaptive responses against the altered self-cell and Granule release.
70
Q

Complement Activation Pathways:

A
  1. Classical
  2. Lectin
  3. Alternative
71
Q

Complements:

A

refers to a group of serum proteins circulating in inactive form (proteins in serum).

72
Q

Once activated, complement plays a role in:

A

-Lysis
-Opsonization
-Inflammation

73
Q

Complement 7 functional categories:

A
  1. Initiators
  2. Enzymatic mediators
  3. Opsonins
  4. Inflammatory mediators
  5. Membrane attack proteins
  6. Complement receptors
  7. Regulators
74
Q

Initiators:

A

Initiate specific rxns after binding soluble or membrane-bound molecules.

75
Q
  1. Enzymatic mediators:
A

Proteolytic enzymes or zymogens (cleave proteins).

76
Q
  1. Opsonins:
A

Bind covalently to microbial cells and serve as ligands for phagocytic cells. (Coat for tasty)

77
Q
  1. Inflammation mediators:
A

Anaphylatoxins cause vascular permeability and leukocyte chemotaxis.

78
Q
  1. Membrane attack proteins:
A

Punch holes in the membranes of invading pathogens.

79
Q
  1. Complement receptors:
A

Bind complement and signal specific cell functions (ex: phagocytosis or neutrophil degranulation).

80
Q

Classical and lectin pathway C3 convertase

81
Q

Classical and lectin pathway C5 Convertase:

82
Q

Classical Pathway initiator:

A

Antigen-antibody immune complexes

83
Q

Lectin pathway initiator:

A

PAMP Recognition by lectins (MBL)

84
Q

Alternative Pathway initiator:

A

Fluid-phase C3 convertase

85
Q

Alternative Tickover Pathway C3 Convertase:

86
Q

Alternative Tickover Pathway C5 Convertase:

87
Q

Alternative Tickover Pathway activator:

A

(Bound) C3b

88
Q

Lectin Pathway activator:

A

MASPs (MBL- associated serine proteases)

89
Q

Classical Pathway activator:

90
Q

C3b Complement Protein (our major Opsonin)

A
  1. Opsonization
  2. Antigen-antibody complexes
  3. C5 convertase
91
Q
  1. Opsonization:
A

C3b binds covalently to microbial surfaces, providing a “tag” allowing recognition by phagocytosis.

92
Q
  1. Ag-Ab Complexes:
A

C3b can attach to the Fc portions of Abs allowing for phagocytosis or movement to liver for elimination.

93
Q
  1. C5 convertase:
A

C3b can bind to complement protein complexes to form C5 convertase.

94
Q

C5 Convertase cleaves C5 and C5 initiates:

A

generation of the Membrane Attack Complex (MAC).

95
Q

Complent Receptors mediate fxn of complement by acting as _________ between the components and the cells which they bind

96
Q

What are the two complement receptor bridges:

A

CR1 and CR2

97
Q

C3aR/C5aR: Granulocytes

A

Binds to C3a and C5a.

98
Q

C3a and C5a act as ___________

A

anaphylatoxins or inducers of inflammation.

99
Q

Complement enhances host defense against infection through:

A
  1. MAC- induce lysis/death (downstream of C5b)
  2. C3b - mediated phagocytosis
  3. Inflammation - C3a and C5a

Immunology (2 decks)

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