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IMIN 200 > Immunology > Flashcards

Immunology Flashcards

1
Q

Why can most invertebrates clear infections but be soon susceptible again?

A

they have no immunological memory

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2
Q

Variola major

A

smallpox; ~50% mortality

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3
Q

Variolation

A
  • China; dried & powdered smallpox scabs used to immunize people; blown into nasal passage; 1-2% mortality +inflammation
  • knowledge traveled the Silk Road to the Ottoman empire (Turkey) and Africa; African slaves introduced it to American and Lady Monatagu saw from Turkey and brought it to England
  • Edward Jenner; cowpox; no mortality + less inflammation
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4
Q

Types of vaccines

A
  • Attenuated (living but weak); ex: cowpox
  • Inactivated (killed whole pathogen)
  • Subunit (parts or components of a pathogen)
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5
Q

Vaccination risks

A
  • Anaphylaxis (allergic response); involves two or more body systems like hives and difficulty breathing
  • Vaccine quality or handling errors
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6
Q

Reproduction ratio (without vaccination)

A
  • Ro
  • transmissibility
  • # of new infections caused by each infected person
  • if high number, pathogen is highly transmissible
  • Ro < 1 = not an epidemic and infection will die out in population
  • Ro > 1 = epidemic and infection will spread in a susceptible host population
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7
Q

Herd immunity

A
  • the proportion of a population that needs to be immune to prevent pathogen spread (achieved by infection or vaccination)
  • based on Ro
  • proportion to vaccinate = 1-1/Ro
  • the more easily transmissible, the higher the population proportion that needs to be immunized to prevent spread (more infectious = vaccinate higher proportion of population)
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8
Q

How do we determine Ro values?

A

Case tracing!

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9
Q

Viral entry routes

A
  • Conjunctiva (measles, coronavirus, rhinovirus, influenza, herpes virus)
  • Respiratory tract
  • Alimentary tract; oral-fecal (poliovirus)
  • Urogenital tract, Anus; sexually transmitted ( HIV, herpes virus)
  • skin, scratch injury, contact w/ blood/secretions (Hep B, rabies, ebola)
  • capillary
  • arthropods (West Nile virus, yellow fever)
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10
Q

Physical and chemical barriers to infection

A
  • mucus and intact mucus membranes
  • enzymes in mucus, tears, and saliva (pH 4.5-6)
  • acid in sweat and sebum
  • acid in stomach (pH 2)
  • antibacterial proteins and zinc in semen
  • competition from commensal bacteria in gut and genital tract
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11
Q

Skin covers ~2 m squared whole mucous membranes cover …

A

~400 m squared

  • thin, permeable barriers
  • gas exchange, food absorption, reproduction
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12
Q

Mucus

A
  • goblet cells: secrete mucus and traps microbes
  • ciliary escalator: cilia push bacterial cells back up; bacteria trapped by mucous and coughed out or swallowed and killed by stomach acid
  • mechanical removal: coughing, sneezing
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13
Q

T or F. Generally, areas of higher moisture contain higher populations of normal flora

A

T (respiratory tract and gut)

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14
Q

Microbial antagonism

A

normal flora inhibits colonization by pathogenic microorganisms through occupation of habitat and competition for resources

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15
Q

Define chemical barriers

A

enzymes that can degrade microbial cell walls in saliva and anti-microbial peptides (AMPs)

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16
Q

AMPs

A

part of innate immune system; can punch holes in microbe membranes; part of an ancient defense system (found in so many organisms)

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17
Q

where are ‘captured’ pathogens taken?

A
  • to closest lymph node or to spleen (screens blood) where circulating lymphocytes transit to see if they recognize it
  • lymph goes through lymph nodes for surveillance of tissues whereas surveillance of blood occurs by blood moving through the spleen
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18
Q

1st line of defense

A

skin, mucous membranes, chemicals, AMPs

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19
Q

2nd line of defense

A

phagocytosis, complement, interferon, inflammation, fever

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20
Q

3rd line of defense

A

lymphocytes, antibodies

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21
Q

Complement factors

A

assemble in the membranes of the pathogens or cell walls sometimes of the pathogen and these can punch holes in the pathogens (rendering them unable to infect)

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22
Q

Interferons

A

once released (when an innate immune cells recognizes a pathogen), alerts other immune cells (whether innate or adaptive) that there is infection in an are! Can lead to recruitment of other cells (innate or adaptive)

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23
Q

Fever

A

can be induced ; systemic response by a local infection; # of pathogens like LOWER temps …; increase temp in mucosal areas and something like flu doesn’t have a chance

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24
Q

Fundamentals of Innate Immunity

A
  1. protective mechanism BEFORE infection
  2. rapid responses encoded within the germline (DNA in egg and sperm cells)
  3. Responses are typically identical upon repeat infection
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25
Q

Lymphocytes that are already armed to take on pathogens without any kind of long-term stimulation

A

NK cells

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26
Q

Mobilizing bodily defenses at sites of infection

A

Inflammation

  • vasodilation
  • increase in capillary permeability
  • influx of immune cells to affected tissues
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27
Q

Four signs of inflammation

A
  • redness: vessels dilate and blood volume increases; allows a lot more of innate immune cells to be in this area ; when there is an infection, there will be signals that tell them to stop at a certain place and enter tissues at dilated capillaries!
  • heat: increased blood volume brings warmth to affected tissues
  • edema: swelling due to accumulation of fluid from blood in affected tissue
  • pain: some inflammatory mediators trigger the pain response ; alters function
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28
Q

Evidence of inflammation

A
  • Elie Metchnikoff (1800s)
  • insult to star-fish larvae
  • rapid localization of cells to site of insult
  • breakdown of thorn by cells
  • first observation of process known as phagocytosis
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29
Q

Mast cells

A
  • first responders

- vacuoles with lots of enzymes that can be secreted to attack pathogens

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30
Q

Neutrophils

A

highly representative in blood; very often first to deal with pathogens; move towards higher concentration of chemicals where infection is at (chemotaxis)

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31
Q

Describe phagocytosis

A

After bacteria are recognized, cell membrane of neutrophils extend on either side of bacteria and bacteria are being bound by receptors on neutrophils and extensions of plasma membrane of neutrophil surrounds bacteria and ultimately, bacteria are endocytosed (membrane forms a vesicle around the bacteria that then parts way from PM and becomes an endosome)
-> phagocytic cells = lysosomes (from golgi); neutrophil has the endosome fuse with lysosome and contents of lysosome (enzymes) are released into the endosome and attack pathogen
THEN two fates: -> phagolysosome (lysosome plus endosome) will fuse with PM and secretion of garbage that’s left over (after the lysosomes degrade)
-> OR phagolysosomes simply degrades the components COMPLETELY ; and can come back and have further rounds of fusion

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32
Q

T or F. Phagocytosis is highly conserved throughout evolution

A

T

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33
Q

Examples of phagocytes

A

macrophages, monocytes, neutrophils

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34
Q

Phagocytosis process

A
  1. phagocytes detects and engages microbe
  2. microbe engagement initiates cytoskeletal rearrangements that drive phagocytosis
  3. the microbe is internalized in a phagosome
  4. phagosome fuses with lysosome = phagolysosome
  5. lysosomal enzymes destroy ingested microbes
  6. reactive oxygen and nitrogen intermediates destroy microbial proteins, genomes, and walls (Reactive O2 and N2 intermediates are very oxidative and attack various products of the microbe and render them useless and destroyed )
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35
Q

Macrophage development

A
  1. like all blood cells, macrophages arise from undifferentiated stem cells in the bone marrow
  2. some stem cells differentiate into short-lived monocytes that circulate in the blood
  3. inflammation recruits monocytes to sites of infection where they differentiate into resident macrophages
  4. resident macrophages are long-lived ‘professional’ phagocytes that ingest large amounts of extracellular material
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36
Q

Phagocytes don’t just eliminate microbes. They …

A

activate neighbouring cells through the release of cytokines and chemokines

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37
Q

Cytokines

A

secreted proteins that drive immune and inflammatory reactions
innate = cytokines are produced by macrophages and NK cells

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38
Q

Induce proteins in the endothelium that make the endothelium more adherent for passing leukocytes

A

Cytokines

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39
Q

Chemokines

A

large family of structurally related, low molecular weight cytokines that stimulate leukocyte movement and regulate the migration of leukocytes from the blood to tissues

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40
Q

T or F. Inflammation is always good!

A

F, NOT all inflammation is good - inflammation may not stop at the end of an immune response or injury = chronic inflammation; results in disorders

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41
Q

The first step in innate immunity

A

detection of microbes by resident cells

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42
Q

This triggers inflammation at the site of infection

A

Microbe engagement

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43
Q

These contain granules and can release them upon recognition of inflammation/pathogen

A

Eosinophil, Basophil, and Neutrophils

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44
Q

Primary APC for priming T cells

A

Dendritic cells

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45
Q

Immune response mediated by B and T lymphocytes to infectious agents and non-infectious molecules

A

Adaptive Immunity

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46
Q

Innate vs Adaptive Immunity

A
  • detects common microbial structures vs vast repertoire of molecules
  • receptors encoded in the germline vs receptors generated by somatic recombination
  • same response upon repeat exposure vs improved “adapted” response to repeat exposure
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47
Q

Types of antigens recognized by B cells

A 
proteins
lipopolysaccharides
lipids
nucleic acids
**broader spectrum than T cells
48
Q

Types of antigens recognized by T cells

A

peptides derived from proteins

49
Q

APCs

A

primary dendritic cells, also macrophages

-> induces T cell response

50
Q

Humoral Immunity

A
  • directed against extracellular microbes
  • mediated by B lymphocytes
  • B lymphocytes secrete antibodies that neutralize and eliminate microbes and microbial toxins
51
Q

Cellular Immunity

A
  • directed against intracellular microbes
  • mediated by T lymphocytes
  • T lymphocytes activate phagocytes and lymphocytes
  • or kill infected host cells
52
Q

T or F. B cells remain naïve circulating blood or lymph nodes awaiting to encounter a pathogen, be activated, and then secrete pathogens

A

T!

53
Q

Cytokines activated by T cells

A

goes to phagocytes; improves phagocytes ability to kill microbe

54
Q

Granzymes

A

endosomal comportment contain enzymes (dysregulate cytochrome C) that can be secreted by killer cell and be deposited in target and end up triggering host cell to commit suicide (effective for killing reservoirs – cells actively producing pathogens)
- cytotoxic and natural killer cells

55
Q

Phases of the Immune Response

A
  1. Recognition: Naive lymphocytes recognize corresponding antigen
  2. Activation: Lymphocytes differentiate and start clonal expansion
  3. Effector phase: differentiated lymphocytes initiate microbial elimination
  4. Decline: after microbial elimination, the signal for lymphocyte activation disappears; most cells activated by antigen die by a process of programmed cell death (apoptosis)
  5. Memory: the remeaning cells are memory lymphocytes, which may survive for months or years; remain in bone marrow or circulate
56
Q

Activation requires two signals:

A

Signal 1 - Antigen receptor binds antigen
Signal 2 - microbial or innate immune signals are also required for lymphocyte activation
**both signals required

57
Q

T or F. We have millions of B cells, each with its own unique BCR and each BCR recognizes a limited number of antigens

A

T

58
Q

T or F. There is a lag time with adaptive immunity reaction after second exposure.

A

F; Memory response - no lag (memory cells already differentiated) also encountering antigen a second time, lag is much shorter bc they proliferate much faster (compared to naïve cells) ; just inherently better cells at producing antibodies

59
Q

What do BCRs recognize?

A

recognize distinct microbial 3-dimensional structure;
B cell that has never previously encountered its target structure (naive) has BCR that is restricted to the plasma membrane of B cell

60
Q

What does B cell activation result in?

A
  • clonal expansion
  • differentiation into effector cells that actively secrete antibodies
  • BCR is modified in such a way that the BCR is secreted as an antibody
61
Q

Functions of antibodies

A
  • released into circulation and mucosal fluids by B cells upon infection
  • neutralized microbes and microbial toxins
  • stops microbes from gaining access to or colonizing host cells
  • does NOT have access to intracellular microbes
62
Q

APCs reside in…

A

potential sites of microbe entry = skin, GI tract, respiratory tract, etc.

63
Q

What do APCs do?

A

capture, process, and present antigens to T lymphocytes in peripheral lymphoid tissues

64
Q

T or F. Just like B cells, each T cell expresses a unique TCR

A

T, they also require co-receptors to assist antigen recognition

65
Q

Two major subsets of T lymphocytes

A
  • CD4+ helper T cells detect antigens presented by professional APCs; secrete cytokines to activate other components of the immune response (macrophages, B cells, etc.)
  • CD8+ cytotoxic T cells detect microbial antigens presented by all nucleated cells and destroy the presenting cells
66
Q

Which cells will clean up after killer cells?

A

Macrophages

67
Q

How do you bring the right lymphocyte together with its cognate antigen upon infection quickly enough to activate the appropriate immune reply?

A
  • the peripheral lymphoid organs (lymph nodes, spleen, mucosal and cutaneous lymphoid tissues) concentrate antigens and lymphocytes to optimize interactions
  • Lymphatics will take fluid from tissues and drain them into lymph nodes
  • Antigens coming by APCs via lymph into lymph nodes and the lymphocytes are coming into lymph nodes from blood = interaction!!!
  • Spleen = lymphocytes can circulate here from blood to potentially encounter APCs
68
Q

A network that transports fluids from tissues through lymph nodes and ultimately to the circulatory system (initially to veins)

A

Lymphatic system

  • excess interstitial fluid is collected by the lymphatic system and is processed by lymph nodes prior to being deposited into the circulatory system
  • unlike circulatory system, the lymphatic system is not closed and has no central pump
69
Q

What happens in the lymphatic system?

A
  1. APCs drain from peripheral tissues into lymph nodes
  2. T lymphocytes enter lymph nodes
  3. APCs activate T lymphocytes
  4. Lymphocytes exit lymph nodes and enter circulation, then exit circulation into inflamed tissue where they mediate microbial destruction
70
Q

Lymph node Cortex

A

B cells concentrated here; they can aggregate into the centers (germinal centers)

71
Q

Lymph node Paracortex

A

combo of T cells and dendritic cells and these APCs can get into all of the areas to present antigens

72
Q

Lymph node Medulla

A

area where cells can enter into efferent lymphatic vessel and head out into circulation

73
Q

Lymphocytes in the lymph nodes, what happens?

A
  • where they encounter APCs
  • activated there and differentiate as well
  • exit lymph nodes and enter circulation, head to inflamed tissues where they mediate microbial destruction
74
Q

Where do APCs capture antigens?

A

in tissues
- they transport these Ags to peripheral lymphoid tissues (lymph nodes usually) where lymphocytes are concentrated to present those Ags to T cells

75
Q

T or F. Dendritic cells will either carry intact Ags for B cells or process fragments for T cells

A

T! -> happens in lymph nodes

76
Q

T cell antigens are _______ peptides bound and presented by ___ molecules

A

linear; MHC

77
Q

collection of genes found in all mammals that code for MHC molecules

A

MHC locus; the locus contains two sets of highly polymorphic genes (class I and II)

78
Q

MHC locus originally discovered as…

A

principle determinant of graft rejection

79
Q

Class I vs Class II MHC-expressing cell types

A

Class I - all nucleated cells; CD8+; Cytotoxic; can kill any virus-infected cell

Class II - Professional APCs (B cells, dendritic cells, macrophages); CD4+; helper T; can also express Class I

80
Q

MHC Class I Structure

A
  • alpha 1 and 2 form groove/cleft
  • two alpha non-covalently linked to beta 2
  • polymorphic residues located at alpha 1 and 2 domains, thereby affecting peptide binding and T cell recognition
  • alpha 3 domain is invariant and contacts T cell CD8 co-receptor; so only CD8+ T cells respond to class I MHC-bound antigens
81
Q

Antigen Processing by Class I

A
  • microbe growth and reproduction in cytoplasm
  • microbial proteins in infected cells
  • cleaved by proteasome complex
  • class I MHC molecules loosely attached to the transporter associated with antigen presentation (TAP) - cellular pump that drives transport of cytoplasmic peptides into ER
  • peptides pumped to ER lumen by TAP where they connect with class I
  • stable binding = complex sent to surface via Golgi and exocytic vesicles
  • surface = where interact with CD8+ T lymphocytes
82
Q

T or F. The Class I pathway response to extracellular microbes

A

F! Intracellular!

  • presented by Class I MHC molecules on the surface of all nucleated cells
  • TCR activation = T cell differentiation to kill infected cells
83
Q

MHC Class II Structure

A
  • alpha 1 and beta 1 form peptide-binding groove; noncovalently linked
  • polymorphic residues are in the alpha and beta 1 domains affecting peptide binding and T cell recognition
  • beta 2 domain is invariant; contacts T cell CD4 co-recptor; so only CD4+ T cells respond
84
Q

Antigen Processing by Class II

A
  • several means to ingest microbes: PRR binds microbes OR receptors bind antibodies bound to microbes OR APCs sample their environment through pinocytosis
  • go to lysosomes
  • cleaved by lysosomal enzymes = numerous peptides
  • in ER, invariant chain blocks peptide binding groove of MHC II, preventing peptides associating with MHC II in ER
  • class II transported to cell surface in exocytic vesicles
  • endosomal vesicles with microbial peptides fuse w exocytic vesicles; invariant chain degraded and MHC II binds peptides
  • stable binding = go to cell surface
85
Q

Properties of MHC

A
  • Co-dominance: both parental alleles are expressed equally; each indiv can express up to 6 different Class I and 10-20 diff class II molecules
  • Polymorphism: multiple MHC alleles means that at least some members of the population will be able to present any given microbial antigen
86
Q

Features of peptide binding to MHC

A
  • each MHC molecule displays one peptide at a time
  • broad specificity
  • very slow-off rate
  • stable expression requires peptide
  • MHC molecules bind only peptides
87
Q

Co-stimulatory functions of APCs

A
  • APCs present antigens and provide second signals for T cell activation
  • microbial substances stimulate APCs to express costimulators on their surface and secrete cytokines
  • costimulators and cytokines provide second signal that triggers T lymphocyte differentiation
88
Q

Ag-Ab/BCR interactions

A
  1. BCR detect three-dimensional antigens

- B cells are active only against extracellular antigens

89
Q

BCR/TCR Activation

A
  1. antigen receptors associate with cell signalling proteins in BCR/TCR complex
  2. adjacent receptors bind two + antigens = aggregate
  3. cross-linking brings signalling proteins together and initiates signal transduction
  4. same in each clone
90
Q

This drives lymphocyte activation

A

antigen recognition

91
Q

Type of glycoprotein produced by B lymphocytes

A

antibodies (immunoglobulin)

- bind antigen (various 3D shapes) with a high degree of specificity and affinity

92
Q

Antibody consists of four polypeptides:

A
  • two identical light chains
  • two identical heavy chains that for a Y
  • each light chain connected to a heavy chain by a disulfide bond
  • 2 heavy chains connected by disulfide bonds
93
Q

Antibody structure:

A
  • each light chain = one V and one C domain
  • heavy chain each have one V domain and at least 3 C domains
  • each domain folds into a characteristic 3D shape (Ig domain)
  • variable v region varies between clones and is involved in antigen recognition
  • constant c region is conserved among clones and is required for structural integrity and effector functions
94
Q

T or F. Antibodies bind antigens by reversible non-covalent interactions

A

T; still strong!

95
Q

Epitope

A

parts of an antigen recognized by antibody; can be recognized on the basis of sequence or shape

96
Q

Affinity

A

strength with which one antigen-binding surface of an antibody binds an antigen

97
Q

Features of antibody-mediated antigen recognition:

A
  1. antibodies recognize a large array of 3D structures
  2. each clone specific for a single antigen
  3. antigen recognition is mediated by specific domains of the antibody
  4. signalling triggers B lymphocyte activation
98
Q

Ig isotype: 2 molecules that is joined by a j chain

A

IgA

  • j chain facilitates transport of IgA across mucosal epithelia
  • also transfer of IgA to newborns to confer neonatal passive immunity
99
Q

IgD

A
  • function poorly understood
  • restricted to membrane and barely expressed on active B lymphocytes
  • IgD knock-out mice do not have any major defects
  • found on naive B cells; act as a marker for B cell development
100
Q

IgE

A
  • secreted as a monomer
  • binds Fc epsilon receptor on mast/basophilic cells
  • binds allergens and facilitates degranulation
  • protection against parasites
  • possible role in cancer immunity
  • additional C terminal domain – more than IgG (binds Fc epsilon)
101
Q

Ig Isotypes

A

five types of antibodies that differ in their C region ; differs in their physical/biological properties and effector functions

102
Q

IgG

A
  • secreted as monomer
  • most abundant
  • can transfer to fetus
  • neutralization of toxins
  • opsonization for inducing phagocytosis via complement system
  • antibody-dependent cytotoxicity on NK cells
103
Q

Antibody-Dependent Cellular Cytotoxicity (ADCC)

A
  • Fc receptors mediates this
  • IgG binds Ag on surface of target cell
  • Fc gamma receptors on NK cells bind Fc of Ig
  • cross-linking of Fc receptors signals to the NK cell to kill target
  • target cell dies by apoptosis
104
Q

IgM

A
  • pentamer
  • 10 different Ag binding sites
  • J chain for secretion
  • first antibody expressed in mature B cells
  • important for activation of complement pathway (neutralization, phagocytosis)
  • appears early after infection and usually not seen upon re-infection
105
Q

Avidity

A

combined strength of multiple binding site interactions an Ab can make with antigen
-> IgM has greater avidity than IgD as it can bind bind MORe epitopes at once than IgD can

106
Q

IgM only expressed

A

immature B cell

107
Q

T or F. Light chains associate covalently with the heavy chains on the Igs

A

T!

108
Q

2 light gene loci hat can produce light chains

A

kappa and lambda

109
Q

The light chain loci displays a similar organization to the heavy chain locus, except…

A

it lacks any D segment

110
Q

What does the constant region on the Ig structure represent?

A

conserved effector function

111
Q

Stages of B cell development: (5)

A
  1. pluripotent stem cells in bone marrow
  2. mature IgM+ B cell
  3. mature, naive B cell circulate peripheral lymphoid organs
  4. no antigen encounter = apoptosis
  5. antigen encounter (1st signal) = second signal = activation
112
Q

Stages of B cell activation (6)

A
  1. naive B cell - antigen
  2. helper T stimulate B cells
  3. activated B cells = clonal expansion
  4. some differentiate in to antibody secreting plasma cells
  5. others = memory cells
  6. others switch class
113
Q

Terminally differentiated B cell

A

can’t differentiate into anything else; plasma cells

-> cant respond to external signalling b/c dedicated to production (producing soluble IgM)

114
Q

Memory lymphocytes

A
  • produced from naive lymphocytes bc of antigen exposure
  • persist for years (quiescent state)
  • rapidly activated by repeat exposure
115
Q

Class Switching

A

changing of an antibodies constant region

- clone of B cells not committed to make a single Ig isotype forever (all start out as IgM though)

116
Q

These induce rearrangements at the heavy chain locus (constant region)

A

cytokine signals

117
Q

T or F. Class switching also affects the variable region

A

F! Antigen specificity is retained; effector function is what’s changed; usually depending on environment of activated B cell

IMIN 200 (3 decks)

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