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Infection & Immunity > Exam 1: Learning Objectives > Flashcards

Exam 1: Learning Objectives Flashcards

1
Q

What are the major functions of the immune system

A

-distinguishes self vs non-self vs altered self
-wound healing and resolution of infection
-retain information in case of secondary exposure
-tissue homeostasis
-support commensal microbiota

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2
Q

3 major lines of defense

A

Physical barriers
Innate immunity
Adaptive Immunity

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3
Q

Inflammation

A

-Normal immune response to infection or damage
-immune cells activated, recruitment of additional cells and secretion of cytokines

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4
Q

4 cardinal signs of inflammation

A

heat, pain, redness, swelling

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5
Q

Cytokines

A

Proteins secreted by immune cells to communicate and signal with other cells

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6
Q

Two arms of the adaptive immune response

A

B cells: make and secrete antibodies to protect against extracellular pathogens before they invade
T cells: kill intracellular pathogens and produce cytokines

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7
Q

Hematopoiesis

A

Development of immune cells
-occurs in bone barrow

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8
Q

Erythroid

A

Leads to red blood cells (erythrocytes) and platelets

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9
Q

Myeloid

A

Leads to erythroid progenitor cells and white blood cells (neutrophils, eosinophils, basophils, macrophages, dendritic cells, mast cells)

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10
Q

Lymphoid

A

Leads to B cells, T cells, NK cells, and ILCs (innate lymphoid cells)

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11
Q

Two major types of adaptive immune receptors and what they recognize

A

B cells (immunoglobulin/antibody): surface bound and soluble forms, recognizes macromolecules
T cells: only surface bound, recognize peptides

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12
Q

Antigen

A

Any foreign molecule that can be bound by a lymphocyte receptor and initiate an immune response

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13
Q

Two types of T cells

A

CD4+ : helper T cells, produce cytokines, binds peptide-MHC II
CD8+ : cytotoxic T cells, kills target cells, binds peptide-MHC I

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14
Q

Antibodies

A

Soluble form of B cells

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15
Q

Immune-privileged

A

Organs that are excluded from the immune system: brain and eyes

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16
Q

Primary lymphoid organs

A

-Thymus, bursa, peyer’s patches, bone marrow
-Where lymphocytes mature and self-reactive cells are elimated

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17
Q

Secondary lymphoid organs

A

-Tonsils, spleen, lymph nodes, peyer’s patches, bone marrow
-Where lymphocytes encounter and respond to antigens

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18
Q

Entrance for microbial products (antigens) in lymph nodes

A

Afferent lymphatic vessels (via dendritic cells)

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19
Q

Lymphocyte entrance in lymph nodes

A

Blood capillaries to high endothelial venules

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20
Q

T cell zone in lymph nodes

A

T cell area, germinal center

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21
Q

B cell zone in lymph nodes

A

Lymphoid follicle, germinal center

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22
Q

Lymphocyte exit in lymph nodes

A

efferent lymphatic vessels

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23
Q

Entrance for microbial products in spleen

A

Blood via central arteriole

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24
Q

Lymphocyte entrance in spleen

A

Blood via central arteriole

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25
Q

T cell zone in spleen

A

Periarteriolar lymphoid sheath

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26
Q

B cell zone in spleen

A

B cell corona

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27
Q

Lymphocyte exit in spleen

A

Blood via veins

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28
Q

Entrance for microbial products in MALTs

A

Gut lumen via M cells

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29
Q

T cell zone in MALTs

A

Blood capillaries and HEVs

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30
Q

Lymphocyte entrance in MALTs

A

Blood capillaries & HEVs

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31
Q

B cell zone in MALTs

A

B cell follicle

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32
Q

Lymphocyte exit in MALTs

A

Efferent lymphatics

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33
Q

Asplenia

A

-Absence of a spleen
-Can be congenital or acquired
-Highly susceptible to certain infections

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34
Q

Mechanical barriers of the skin, lung, gut, and oral cavities

A

epithelial cells joined by tight junctions
skin & gut: longitudinal flow of air/fluid
lungs: movement of mucus by cilia
eyes/nose/oral cavities: tears, nasal cilia

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35
Q

Autonomic mechanical strategies for expelling pathogens

A

blinking, tears, swallowing, peristalsis, mucociliary escalator

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36
Q

Energetic mechanical strategies for expelling pathogens

A

coughing, sneezing, urination

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37
Q

Violent mechanical strategies for expelling pathogens

A

vomiting, diarrhea

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38
Q

Examples of chemical barriers

A

skin: fatty acids
gut: low pH, antimicrobial enzymes
lungs: pulmonary surfactant
cavities: antimicrobial enzymes
all: antimicrobial peptides

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39
Q

How do defensins function as antimicrobial peptides

A

defensins are amphipathic which allow them to disrupt membrane integrity of pathogens
promote protein unfolding, denaturation of bacterial toxins

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40
Q

How to pentraxins bridge pathogen and immune cells

A

promote engulfment of pathogens by phagocytes

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41
Q

Benefits of commensal microbiota

A

presence of microbiome makes it harder for pathogenic microbes to invade by competing for nutrients and space
required for immune homeostasis and proper barrier function

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42
Q

Complement system

A

complex system of 30+ proteins: kill invading microbes, trigger inflammation, regulate immunity

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43
Q

Complement fixation

A

irreversible attachment of C3b to pathogens

44
Q

C3 activation

A

C3 cleaved unto C3a and C3b
thioester bond exposed
most C3b hydrolyzed by water
some C3b binds to surface of pathogens

45
Q

3 pathways of complement activation

A

Alternative pathway
Lectin pathway
Classical pathway

46
Q

Soluble alternative C3 convertase

A

80-90% complement activation
initiated by spontaneous hydrolysis of thioester bond of C3 to iC3 “tickover”
iC3 binds to B. Bb remains bound, Ba cleaved
resulting complex, iC3Bb functions as soluble C3 convertase

47
Q

Alternative C3 convertase

A

80-90% complement activation
iC3Bb cleaves other C3s into C3a & C3b
C3b fragments bind to pathogen surface
C3b bind to B, produces C3bBb

48
Q

Lectin pathway

A

triggered when MBL or other lectind binds to carbohydrates on microbial surface
MBL binds and activates MASP
MASP activates C4 and C2 to generate classical C3 convertase C4bC2a

49
Q

Classical pathway

A

triggered when antibodies of C-reactive protein bind to bacterial surface and recruits C1 complex
activates C4 and C2 to generate C4bC2a

50
Q

3 downstream outcomes of the complement system

A

Recruitment of inflammatory cells, opsonization of pathogens, perforation of pathogen cell membranes (MAC)

51
Q

Opsonization

A

= engulfment
C3b coated pathogens bound by complement receptor 1 to promote phagocytosis

52
Q

Anaphylotoxin production

A

= inflammatory cells
C3a, C4a, C5a
recruits neutrophils and monocytes to site of infection
also trigger contraction of smooth muscle, mast cell & basophil degranulation leading to histamine release and vascular permeability

53
Q

Membrane attack complex

A

= lyse
perforation of pathogen cell membranes causes assembly of membrane attack complex
forms a pore in the membrane

54
Q

Why are complement regulatory proteins necessary

A

could lead to immune mediated pathology and collateral damage
soluble factors prevent amplification
membrane bound factors prevent formation of C3 convertase & inactivates C3b

55
Q

What are pattern recognition receptors (PRRs)

A

recognized pathogen-associated molecular patterns (PAMPs) presented by microbes

56
Q

Major classes of Pattern Recognition Receptors

A

Membrane bounds receptors:
TLRs- toll like receptors, surface and endosomal
SRs’ scavenger receptors, surface
Cytoplasmic receptors
NLRs- NOD like receptors
RLRs- RIG-I-like receptors

57
Q

TLR1:2 and TLR2:6 heterodimers

A

peptidoglycans
lipoproteins
(surface)

58
Q

TLR3

A

double stranded RNA
(endosomal)

59
Q

TLR4

A

lipopolysaccharide

60
Q

TLR5

A

flagellin

61
Q

TLR7 and TLR8

A

single stranded RNA
(endosomal)

62
Q

TLR9

A

unmethylated CpG DNA
(endosomal)

63
Q

How does assembly of adaptor components lead to intracellular signaling

A

engagement of PRRs leads to intracellular signaling cascade
oligomeric assembly brings weak interactions together quickly

64
Q

Outcome of TLRs

A

NF-kB activation and cytokine production

65
Q

Outcome of SRs

A

phagocytosis of microbes

66
Q

Outcome of NLRs

A

NF-kB activation or cytokine (inflammasome/IL-1beta) production

67
Q

Outcome of RLRs

A

production of type 1 Interferons

68
Q

Difference in response between extracellular and intracellular LPS

A

Intracellular LPS induces death
Extracellular LPS ?

69
Q

What are DAMPs

A

Damage-associated molecular patterns
Products of broken cells
Released by damaged or stressed tissues

70
Q

How do Type 1 interferons amplify the innate response

A

Produce anti-viral proteins
Amplify the response through paracrine action

71
Q

What are the main effector functions of tissue-resident macrophages

A

Sentinels for invasion by pathogens
Produce cytokines
Tissues maintenance

72
Q

What is phagocytosis?

A

Process by which cells ingest or engulf particles or microorganisms

73
Q

Stages of phagocytosis

A

1) binding to pathogen
2) ingestion
3) degradation in endosome/phagosome
4) further degradation in phagolysosome

74
Q

Main effector functions of neutrophils

A

Phagocytosis
Respiratory burst
Production of NETs (neutrophil extracellular trap: capture & kill pathogens w/o ingesting them)

75
Q

Extravasation

A

Leakage of fluid from blood vessel into tissue

76
Q

4 stages of extravasation

A

1) rolling adhesion
2) tight binding
3) diapedesis
4) migration

77
Q

Main effector functions of NK cells

A

Highly cytotoxic
Produce cytokine IFN-gamma

78
Q

How do NK cells recognize altered self

A

NK cells are inhibited by target cell expression of MHC I
Loss of MHC I will lead to killing of infected host cell or tumor cell

79
Q

Difference between mature B cell and plasma cell

A

B cell: antibodies bound to surface
Plasma: secrete antibodies
B cells turn into plasma cells when they encounter an antigen

80
Q

Parts of an immunoglobulin

A

heavy chains, light chains, constant regions, variable regions, hinge region

81
Q

Hypervariable regions

A

Form the antigen binding pocket

82
Q

Epitope

A

Part of the antigen which the antibody binds
Found at end of variable region

83
Q

Affinity

A

Measurement of binding strength of the antibody

84
Q

4 mechanisms to generate antibody diversity

A

Before antigen encounter
1. somatic recombination
2. junctional diversity
3. heavy chain & light chain pairing
After antigen encounter
4. somatic hypermutation

85
Q

Purpose of somatic recombination (VDJ recombination)

A

Produces high diversity in antibody specificity using only a limited number of genes

86
Q

Overall outcome of somatic recombination

A

Variable region sequences constructed from random recombination of a light chain (V+J) and a heavy chain (V+D+J)

87
Q

Steps of somatic recombination

A

1) recombinational signal sequences (RSS) mediate V/J and V/D/J rearrangements
2) recombination-activating genes (RAG-1 & RAG-2) mediate DNA rearrangements
? idk if this is right ?

88
Q

How is recombination regulated

A

12/23 rule: recombination only occurs between a 12 bp spacer and a 23 bp spacer
RAG-1/2 only expressed by B & T cells

89
Q

Junctional diversity

A

Created during DNA rearrangements
Diversity in the hypervariable regions of H & L chains
Consist of P N P nucleotides

90
Q

Somatic hypermuation

A

After contact with an antigen, the rearranged gene segments encoding the variable region undergo many mutations with the goal of increasing affinity to the antibody

91
Q

5 main isotype classes

A

IgG, IgM, IgD, IgA, IgE

92
Q

Isotype switching

A

Antibody changing classes
Involves gene rearrangement between specific switch regions

93
Q

how are monoclonal antibodies generated

A

1) immunized B cells fused with myeloma cells
2) grown in a medium that selects for only hybrid cells to survive
3) select for antigen-specific hybridoma
4) clone selected hybridomas (aka monoclonal antibody)

94
Q

What are monoclonal antibodies used for

A

1) as therapies for large number of diseases (ex. organ transplants, non Hodgkin’s lymphoma, plaque psoriasis, rheumatoid arthritis, covid)
2) detect proteins on cell surface through flow cytometry

95
Q

T cell receptor

A

Membrane bound glycoprotein
Consists of 2 polypeptide chains: TCRalpha & beta or TCRgamma & delta
Two regions: variable and constant

96
Q

How is TCR diversity generated

A

VDJ areas undergo recombination using RAG1/2
Junctional diversity

97
Q

Compare and contrast features of BCRs & TCRs

A

TCR:
Do not undergo somatic hypermutation, isotype switching
Only have 1 antigen binding site
Are not secreted
beta and delta have VDJ, alpha and gamma have VJ
BCR:
Have 2, 4, or 10 binding sites
Do not bind with MHC
Are secreted
Heavy chain has VDJ, light chain has VJ

98
Q

Components of TCR complex

A

cytoplasmic tail, transmembrane region, constant (C) region, variable (V) region, antigen binding site

99
Q

Steps of antigen processing and presentation

A

1 peptide degradation & peptide formation
2) peptide loading onto MHC molecules
3) peptide-MHC complex transport to the cell surface
4) presentation of antigen to T cells

100
Q

Compare and contrast CD4+ and CD8+ T cell recognition

A

CD8+: recognize antigen from infected cells, associated with killer T cells
CD4+: recognize antigens from antigen presenting cells (APCs), associated with helper T cells, make cytokines

101
Q

How are endogenous vs exogenous antigens processed for presentation

A

Endogenous: made by virus infected cells, fragmented by proteasomes, bind to MHC class I, presented to CD8+
Exogenous: captured by antigen presenting cells, fragmented by proteases, bind to MHC class II, presented to CD4+

102
Q

Components of peptide loading complexes for MHC I and MHC II

A

Class I: alpha 1,2,3, beta2m
Class II: beta 1,2 and alpha 1,2

103
Q

Cross presentation

A

Allows CD8+ T cells to recognize antigens presented by non infected dendritic cells
Prevents immune evasion by viruses

104
Q

How is MHC diversity generated

A

genetic polymorphism, many different forms of the gene exist within the human population

105
Q

MHC haplotype

A

Combination of MHC genes on a single chromosome, each individual inherits two parental haplotypes

106
Q

Why is diversity at the MHC locus so important for immunity

A

The more unique MHCs you have, the more antigens you can respond to
Too many loci can lead to autoimmunity

107
Q

What is Devil Facial Tumor Disease and why is it impacted by lack of diversity

A

An infectious tumor found in the tasmanian devil, which are all highly inbred and thus have low MHC diversity. This allowed for the disease to spread to virtually every single tasmanian devi

Infection & Immunity (3 decks)

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