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Immunology Quiz Questions > Exam 3 Bold Words > Flashcards

Exam 3 Bold Words Flashcards

1
Q

guanine-nucleotide exchange factors (GEFs)

A

-phosphorylated by Syk
-catalyze the exchange of guanine nucleotides on guanine nucleotide binding proteins

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2
Q

germinal center

A

-formed by b-cells that have migrated to a lymph follicle
-affinity maturation or become memory cells

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3
Q

inherited immunodefieciency

A

primary immunodeficiency
a disorder that occurs because some part of the immune system is missing or defective due to genetic disorders

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4
Q

acquired immunodeficiency

A

secondary immunodeficiency
a disorder that occurs due to non-inherited factors such as malnutrition, age, infection, disease, drugs, or toxins

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5
Q

combined immunodeficiency

A

these disorders result from impaired b-cell and T-cell production or responses

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6
Q

severe immunodeficiency

A

result from mutations that block the development of immune cells

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7
Q

tolerable immunodeficiencies

A

result from mutations that have limited effects in a select number of cells

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8
Q

most common type of inherited immunodeficiency

A

B cell immunodeficiencies are (1st)
combined immunodeficiencies (2nd)
T-cell immunodeficiencies (3rd)
innate immunodeficiencies (4th)

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9
Q

mutations in RAG1 or RAG2 result in

A

Omenn Syndrome

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10
Q

Omenn syndrome

A

mutations in RAG1 or RAG2
patients lack both T and B cells

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11
Q

People with Omenn syndrome can develop

A

severe combined immunodeficiency (SCID)

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12
Q

mutations in the C5-C9 genes can result in

A

an impaired ability to generate the membrane attack complex (MAC)

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13
Q

in general, b-cells can be activated by

A

an antigen being recognized by an immunoglobulin on the b-cell signals a humoral response from the adaptive immune system

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14
Q

compared to t-cell activation, b-cell activation

A

has signaling events that drive a similar mechanism for activation, division, and differentiation

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15
Q

naive b-cells are activated by

A

-multiple immunoglobulins recognizing an antigen and clustering on the cell surface
-a costimulatory signal is needed for proper activation

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16
Q

what effect does clustering of immunoglobulins have?

A

-crosslinking or clustering initiates signaling events involved in activation
-activity of Ig alpha and beta enable immunoglobulins to relay signals to the cytoplasm

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17
Q

the b-cell coreceptor acts as

A

-the second key
-analogous to CD28 for the t-cell coreceptor

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18
Q

what three polypeptides make the b-cell coreceptor

A

Cr2, CD19, and CD81

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19
Q

the ITAMs on Ig alpha and beta are phosphorylated by

A

Blk, Lyn, and Fyn

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20
Q

ITAMS can serve as what

A

the binding site for signaling molecule

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21
Q

what is Syk and how is it activated

A

Syk is a kinase in b-cells that is similar to ZAP70 in t-cells and is activated through the phosphorylated ITAMs which initiates gene expression changes

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22
Q

how does Syk activate b-cells?

A

-activates PLCgamma which initiates two different pathways
-phosphorylates and activates GEFs

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23
Q

PLCgamma cleaves what into what

A

phosphatidylinositol bisphosphate into diacylglycerol and inositol triphosphate

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24
Q

what three transcription factors promote b-cell proliferation and differentiation

A

NFAT, NFkB, and AP-1

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25
Q

what are two fates of b-cells

A

-differentiation into plasma cells that produce soluble IgM
-migration to a germinal center for affinity maturation or memory cell

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26
Q

how do b-cells migrate to a lymphoid follice

A

chemotaxis from the secretion of CXCL13 (a chemokine) by follicular dendritic cells

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27
Q

what are the two responses for clonal expansion of activated b-cells

A
  1. t-independent
  2. t-dependent
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28
Q

t-independent (ti)

A

thymus-independent

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29
Q

t-dependent (td)

A

thymus-dependent

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30
Q

what b-cells can activate through ti

A

b-1 b cells and marginal-zone b cells

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31
Q

what is the difference between ti-1 and ti-2 antigens

A

-ti-1 antigens bind to an immunoglobulin and a pattern recognition receptor (TLR4) on the b-cell surface
-ti-2 antigens are formed by repetitive unit (LPS) and cause clustering of immunoglobulin receptors

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32
Q

what b-cells are activated through td response

A

b-2 b-cells

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33
Q

td antigens

A

are recognized by the b-cell receptor and MHCII internalizes and processes them before they can be recognized by a t-cell receptor for the same antigen

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34
Q

what other signals are needed from a helper t-cell for activation of a td antigen-recognizing b cell

A

-cytokines such as IL-4
-CD40 ligand on the t-cell interacting with CD40 on the b-cell

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35
Q

what is CD40

A

the second key, b-cell coreceptor

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36
Q

what is the CD40 ligand

A

on the t-cell and binds to the CD40 molecule on the b-cell

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37
Q

how d t and b cells become a conjugate pair

A

-expression of ICAM-1 is induced on the b-cell by binding of CD40 to its ligand
-ICAM-1 binds tightly to LFA-1 on the t-cell

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38
Q

where does b-cell activation occur

A

secondary lymphoid tissue in the t-cell zone

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39
Q

what are the two fates of conjugate pairs

A
  1. migration to the medulla where b-cell differentiate into plasma cells
  2. migration to the medullary cord then the lymphoid follicles for clonal expansion into centrocytes
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40
Q

what is the primary focus

A

where the conjugate pairs are in the medullary cords and b and t cells can undergo clonal expansion

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41
Q

what is the secondary focus

A

where conjugate pairs are in the lymphoid follicle and follicular dendritic cells can provide signals for b-cell activation and proliferation

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42
Q

define aid

A

activation-induced cytidine deaminase
-in the secondary focus
-begins to be expressed when lymphoid tissues swell from cells dividing in the germinal center
-activates somatic hypermutation and isotype switching

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43
Q

how is immunoglobulin affinity maturation driven?

A

somatic hypermutation occurs within the germinal centers and is driven by the activity of AID through cytosine-to-uracil transitions which affects the binding of immunoglobulins on the b cell

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44
Q

how does the binding affinity of immunoglobulins occur

A

deamination of cytosine bases and subsequent DNA repair mechanisms change the original cytosine base to another base

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45
Q

where is the activity of AID

A

it is random toward cytosine bases in the variable regions of the immunoglobulin genes so there is either a positive or negative effect on the affinity of immunoglobulins for their antigens

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46
Q

what cells in the germinal center can present antigens to centrocytes and what does this do

A

-t-cells, follicular dendritic cells, and macrophages
-promotes additional round of positive and negative b-cell selection after somatic recombination has occurred

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47
Q

how does positive selection occur in germinal centers

A

-follicular dendritic cells present antigens to the immunoglobulins of centrocytes
-BAFF survival signals are gained by b-cells with a high enough affinity
-the bound antigen from the follicular dendritic cell is processed and present to helper t-cells
-helper t-cells provide survival signals to b-cells and express BcI-XL to prevent apoptosis

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48
Q

how is apoptosis of a b-cell in a germinal center with an altered immunoglobulin prevented

A

binding to both the follicular dendritic cell and helper t-cell

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49
Q

what do b-cells that are bound to follicular dendritic cells and helper t-cells in the germinal center differentiate into

A

plasma cells or memory cells

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50
Q

what happens if the altered immunoglobulin recognizes self-antigens

A

negative selection to remove or inactive the b-cell to prevent autoimmune disease

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51
Q

how is isotype switching driven and where does it occur

A

-occurs in the germinal center of the follicle
-cytosine deamination in the switch region of the immunoglobulin heavy chain loci

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52
Q

why is single-stranded DNA required for AID activity

A

AID can only act on DNA regions that are actively undergoing transcription or replication

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53
Q

what cytokines from helper t-cells can promote isotype switching

A

IL-4, IL-5, and TGF-beta
-they direct transcription at certain switch regions so that AID can target specific cytosines for proper isotype switching

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54
Q

what are some major immunoglobulin functions for fighting pathogen infection

A

-neutralization
-protection of internal tissues
-activation of innate immune cells
-complement activation
-clearance of small immune complexes

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55
Q

what do neutralizing antibodies do and why are they important

A

-they can prevent pathogens from interacting with target cells by interacting with the toxins and cell-surface molecules on pathogens
-this prevents toxin action and blocks pathogen entry into cells
-important for viruses

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56
Q

how are the isotypes of b-cells determined

A

by the Fc region for the constant region of the heavy chains

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57
Q

what do Fc receptors do

A

Fc receptors on innate immune cells bind to immunoglobulins and enhance the function of the cells

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58
Q

FcgammaRI

A

receptor on neutrophils that allow phagocytic cells to bind to the Fc portion of an immunoglobulin

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59
Q

how are pathogens tagged for removal by phagocytic cells

A

Fc receptors (FcgammaRI) that recognize IgG are expressed by macrophages and neutrophils that have opsonized a microbial surface and the receptor binds to the Fc portion of an immunoglobulin

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60
Q

what are examples of granulocytes

A

mast cells, basophils, and eosinophils

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61
Q

what do granulocytes do

A

expel pathogens from the body by activating inflammatory responses and muscle contraction for sneezing, coughing, etc.

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62
Q

inflammatory mediators

A

-histamine
-typically IgE
-secreted by activated granulocytes
-trigger expulsion mechanisms

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63
Q

what response do granulocytes work with

A

humoral adaptive immune response

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64
Q

how are histamines released

A

degranulation of mast cells caused by cross linking

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65
Q

what receptor does IgE tightly associate with

A

FcepsilonRI

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66
Q

how many different IgE immunoglobulins can a single granulocyte bind to

A

many different IgE immunoglobulins because there are multiple FcepsilonRI receptors on a granulocyte

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67
Q

why are natural killer cells important

A

they play an important role in the recognition of intracellular infection

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68
Q

antibody-dependent cell-mediated cytotoxicity

A

how nk cells target cells they bind are their FcgammaRIII receptor has coated them in IgG

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69
Q

how is the adaptive immune system able to recognize a wide variety of pathogens

A

-the diversity of t and b-cell receptors
-clonal selection of lymphocytes allows them to target and clear an infection
-memory cells from the primary immune response remember the specific pathogen

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70
Q

how long does it take the primary response to resolve infections

A

up to 14 days
-b-cell activation must be activated
-immunoglobulin isotypes are limited

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71
Q

how long does the secondary immune response take

A

3-4 days
-due to the differentiation and action of memory cells

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72
Q

what is the pattern of IgM and IgG during the primary response

A

IgM: increases around 11 days, reaches a peak at 14 days, then decreases
IgG: begins to increase around 14 days, reaches a peak at 21 days that is higher than IgM, then decreases

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73
Q

what is the pattern of IgM and IgG during the secondary response

A

IgM: increases around 4 days and has returned to basal levels before 10 days with a very small peak
IgG: increases around 3-4 days with IgM and reaches its peak around 14 days, then begins to slightly decreases, intensity of peak is the highest

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74
Q

what do memory cells that were produced from the primary immune response do

A

-respond quickly to a second exposure
-produce immunoglobulins that have undergone somatic hypermutation and isotype switching
-monitor for antigens in various tissues

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75
Q

what is the role of long-lived memory cells

A

trigger the rapid adaptive immune response upon exposure to their recognized pathogen

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76
Q

how are memory t-cells different from naïve t-cells?

A

-different cell-surface molecules are expresses
-populate different locations
-activated by different antigen presenting cells

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77
Q

what are the four subpopulations of memory t-cells produced during a primary adaptive immune response

A

-t memory stem cells (tscm)
-central memory t cells (tcm)
-effector memory t cells (tem)
-resident memory t cells (trm)

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78
Q

what can tscm’s differentiated into

A

tcm and tem

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79
Q

where are tscm’s found

A

circulatory and peripheral tissues like the lymph node

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80
Q

what is special about tscm’s

A

they have the potential for high survival, self-renewal, and multipotency for other memory t cells

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81
Q

where can tcm’s be found

A

circulatory but mostly lymphatic systems

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82
Q

what does tcm’s expression of IL-2 do

A

allows them to activate and differentiation into effector cells after exposure to specific antigen

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83
Q

where are tem’s found

A

secondary lymphoid tissues and circulatory and lymphatic systems

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84
Q

what does secretion of IFNgamma and TNFalpha do for tem’s

A

allows them to quickly activate and differentiation into effect t cells in peripheral tissues without the need to migrate through secondary lymphoid tissues

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85
Q

where are trm’s found

A

they reside within a peripheral tissue and do not leave so they can offer protection against recurring infection

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86
Q

what cell-surface markers are used to differentiate naïve and memory t cells

A

-chemokine receptor CCR7
-L-selectin (CD62L)
-CD103

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87
Q

what do activated b-cells within germinal centers produced

A

effector plasma cells responsible for secreting high-affinity, isotype-switched immunoglobulins

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88
Q

where do memory b-cells localize

A

the spleen

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89
Q

what does IgG produced by a reactivated memory b-cell do

A

-inhibits naïve b-cells from undergoing activation
-opsonizes the pathogen

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90
Q

variolation

A

-used the variola virus (smallpox)
-developed by edward jenner
-used pustule fluid
-worked as well as vaccination but caused smallpox in 1%

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91
Q

vaccination

A

-used the vaccinia virus (cowpox)
-cross protects against small pox
-worked as well as variolation but was less risky

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92
Q

the covid-19 vaccines developed by Pfizer/BioNTech and Moderna are

A

mRNA vaccines

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93
Q

how were covid vaccines able to developed, tested, and produced within 11 months

A

the coronaviruses that caused SARS in 2002-2004 and COVID-19 in 2020 were very similar so research was already being conducted

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94
Q

do vaccines cause autism

A

no, the 1998 study by Andrew Wakefield published in the Lancet that linked the MMR vaccine to autism faked all of its data and was eventually redacted (I wrote like two whole pages in an essay about the anti-vaccine movement about this study and the impact it has had)

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95
Q

what is the strategy behind vaccines

A

inducing a primary immune response that promotes the activation of the exact lymphocytes needed to combat the actual pathogen

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96
Q

what is the goal of vaccination

A

production of memory b and t cells

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97
Q

why does vaccination not provide absolute protection

A

“microbes can always find a way to get around your defenses” - dr. franklund

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98
Q

what are inactivated vaccines

A

killed or inactivated pathogens that are still antigenic but the virus can no longer replicate, which makes them ‘safer’

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99
Q

what are live attenuated vaccines

A

-utilize pathogens that have lost their ability to cause disease but are still alive
-the pathogen lives inside the host and allows the vaccine to mimic an infection
-provides IgA protection but can still mutate which is bad

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100
Q

is one dose enough for an inactivated vaccine to provide proper protection

A

no, booster doses are often required in order for an immune response that provides a high enough level of protection to be elicited

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101
Q

is one dose enough for a live attenuated vaccine to provide proper protection

A

yes, the vaccine closely mimics an infection so a robust immune response is produced with one dose

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102
Q

what are toxoid vaccines

A

vaccines that neutralize toxin products expressed by pathogens via immunoglobulin production

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103
Q

why can toxins for toxoid vaccines not be injected in their natural form

A

as much as 1 ng will kill you

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104
Q

how does a toxin become a toxoid

A

inactivation by formalin or heat treatment so they can be used in a toxoid vaccine

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105
Q

what are subunit vaccines

A

vaccines that raise a primary immune response to protect against pathogen adhesion molecules and prevent their entry into target cells

106
Q

what are conjugate vaccines

A

multivalent vaccines that join a weak antigen (carbohydrate/polysaccharide coat) to a strong antigen (protein/toxoid) to produce multiple epitopes

107
Q

what type of response is created by conjugate vaccines in adults

A

a t-independent response that produces opsonizing antibodies

108
Q

what are recombinant vector vaccines

A

a vector (harmless bacteria or attenuated virus) has a plasmid for a pathogen antigen inserted and begins to express the antigen which leads to an adaptive immune response to the pathogenic antigen

109
Q

what are dna vaccines

A

vaccine is placed directly into the host where is it picked up and incorporated into their genomic DNA, a vector is not used

110
Q

what are messenger rna (mrna) vaccines

A

an mrna encoding an antigen target is delivered to a target cell which uptakes the mrna and translates the antigen to induce an adaptive immune response

111
Q

what does a vaccine need to do to be effective

A

-promote clonal selection of lymphocytes that will be protective against a pathogen
-ensure that these lymphocytes receive a proper costimulatory signal

112
Q

why is the induction of an inflammatory response good for a vaccine

A

it is needed in order to active expression of the costimulatory signal B7 (the 2nd key) on dendritic cells which is necessary for activation of naïve t cells

113
Q

what is an adjuvant

A

an additive (ex-metals) to a vaccine that induces inflammation to strength the immune response

114
Q

questions that must be addressed in developing a vaccine

A

-can the antigen revert to being pathogenic (saben polio vaccine)?
-can the antigen induce toxicity (cross reactivity)?
-are the adjuvant components safe in humans?
-was the vaccine developed in an organism that may induce an allergic response

115
Q

what are modes of delivery for vaccines

A

-most are injected intramuscularly
-some can be inhaled (flumist)
-live attenuated rotavirus vaccines is given orally

116
Q

what is the mucosa

A

-mucous membrane
-thin sheet of tissue that secretes mucous and lines body structures in respiratory, GI, and genitourinary tracts
-important front line for immune system to monitor for pathogens

117
Q

what does the systemic immune response do (general)

A

innate and adaptive responses the protect most of the body produce an inflammatory response

118
Q

what does the mucosal immune response do (general)

A

maintain mucosal barrier to prevent contact between environments

119
Q

what is mucus

A

thick viscous fluid covering mucosae that lubricates and protects mucosal surface

120
Q

how does mucus prevent microbial colonization

A

proteoglycans and glycoproteins work with peptides and enzymes to inhibit pathogens

121
Q

what are mucins

A

family of glycoproteins secreted by epithelial cells that allows for o-linked glycosylation (ser and thr) that increases the molecular weight and viscosity to inhibit the movement of pathogens

122
Q

what does mucosa-associated lymphoid tissue (malt) do

A

promote antigen delivery to circulating lymphocytes to ensure protection of mucosal barriers

123
Q

what is the function of malt’s

A

centralize activation of an adaptive immune response at mucosal surfaces

124
Q

where are malt’s located

A

beneath epithelial cells, sometimes referred to as inductive compartment

125
Q

what are different types of malts

A

galt
balt
calt
nalt

126
Q

what are galt’s

A

-gut-associated lymphoid tissue
-activated lymphocytes and macrophages residing in connective tissue below mucosal epithelia

127
Q

how is the lamina propria important to galt’s

A

the connective tissue that is also referred to as effector compartment and contains immune effector cells such as b, t, macro, and dendritics

128
Q

what are peyer’s patches

A

aggregated lymphoid nodules that are aggregations of galt in small intestine

129
Q

what do isolated lymphoid follicles of the gi tract contain

A

b cells

130
Q

how does the gut microbiota help us

A

-compete with pathogens for space and nutrients
-aid in digestion and produce important vitamins
-produce metabolic products and antimicrobial agents
-may be responsible for development of mucosal immunity
-act as a sparing partner to keep the immune system stimulated

131
Q

how does the microbiota help the lamina propria

A

help develop TH17 helper t cells, which are a major cell in the lamina propria

132
Q

how are interactions between the microbiota and epithelial cells limited

A

-mucus, mucins, IgA, and antimicrobial peptides
-tight junctions between cells that prevent migration of microorganisms

133
Q

what are danger associated molecular patterns (damps)

A

-raw nucleic acids
-heat shock proteins
-cytokines
-plasma membrane proteins (sign of cell lysis)

134
Q

what are microfold cells (m cells)

A

epithelial cells that ‘quietly’ deliver antigens to galt via transcytosis

135
Q

how do m cells do transcytosis

A

the luminal side of the m cell binds the microorganism, engulfs it, and transports it to the apical side facing galt

136
Q

what is the intraepithelial pocket

A

formed by extensive folding and provides location for antigen delivery

137
Q

how do dendritic cells deliver antigens to malt in the lamina propria

A

projections are extended through the barrier and bind to pathogens in the gut lumen, then take them up and process them before they are moved to malt or mesenteric lymph node for antigen presentation

138
Q

how do mucosal epithelial cells utilize tlr’s

A

toll-like receptors recognize pathogens and activate NFkB, produce the inflammatory cytokines IL-1 and IL-6, produce antimicrobial peptides and chemokines

139
Q

what is nod

A

a family of intracellular proteins that bind bacterial cells wall components and activates a signaling cascade

140
Q

NOD1 and NOD2 are present where

A

mucosal epithelial cells

141
Q

what innate immune cells are present at mucosal surfaces

A

-intestinal macrophages
-gut dendritic cells
-innate lymphoid cells

142
Q

what do intestinal macrophages do

A

-remove microorganisms in the lamina propria via phagocytosis
-prevent damage to the mucosal surface due to their lack of inflammatory cytokines such as TNFalpha, IL-1, and IL-6

143
Q

how is oral tolerance provided

A

by gut dendritic cells that take up digested food and activate Treg cells that recognize commensal and foreign pathogens

144
Q

why is oral tolerance important

A

foreign antigens encountered during digestion pose no disease threat and we need to be able to eat

145
Q

what are some innate lymphoid cells

A

ILC1, ILC2, ILC3

146
Q

what does ILC1 do

A

activate macrophages and dendritic cells by secreting IFNgamma

147
Q

what does ILC2 do

A

secrete cytokines like IL-5 to promote activation of granulocytes and respond to proteins produced by helminth infection

148
Q

what does ILC3 do

A

secrete cytokines IL-22 (epithelial cell antimicrobial peptide secretion) and IL-17 (neutrophil activation)

149
Q

why do naïve b and t cells leave malt

A

CCL19 and CCL2 that bind CCR7 receptor are secreted by secondary lymphoid tissues and if they do not find antigen they migrate to different lymphoid tissues

150
Q

what makes up the heterogenous t cell population

A

-alpha:beta or gamma:delta
-CD4 or CD8

151
Q

where are plasma cells and what immunoglobulin do they secrete

A

80% are in mucosal tissue and secrete mostly IgA but can secrete IgM, IgG, and IgE

152
Q

what two immunoglobulins neutralize pathogens at mucosal surface and why

A

IgA and IgM, they have multiple binding sites

153
Q

what is the difference between IgA and IgM

A

IgM: pentameric, 10 binding regions, able to activate complement through classical pathway
IgA: dimeric, 4 binding regions, serves as neutralizing antibody, cannot activate complement

154
Q

what is different in the IgA subclasses

A

the hinge region connecting Fab and Fc region of the heavy chain

155
Q

what is the difference between the IgA subclasses IgA1 and IgA2

A

IgA1: longer and more flexible hinge region is able to bind multiple epitopes on a single pathogen
IgA2: shorter and less flexible hinge region is more resistant to protease cleavage from pathogens

156
Q

what are some of the mucosal infections people with a selective IgA deficiency are susceptible to

A

-sinus infections
-respiratory infections
-GI infections
-chronic diarrhea

157
Q

how would you describe an IgA defficiency

A

“hypersensitive and hypersusceptible” - dr. franklund

158
Q

how do effector t-cells fight helminth infection

A

increase helminth shedding when CD4 cells activated are Tfh and Th2 cells that activate IgE producing plasma cells and cytokines

159
Q

what are some tactics that pathogens use to evase the immune system

A

-genetic variation leading to changes in surface molecules
-mimicking host molecules
-hiding in host cells
-altering the host immune response by producing substances such as toxins or superantigens
-competing against the host to survive and multiple despite the innate and adaptive immune responses

160
Q

how pathogens evade the immune system through genetic variation

A

because the immune system recognizes through receptors or antibodies, pathogens can mutate to change their surface to avoid detection by the immune system

161
Q

what antigen is in LPS

A

o-antigen

162
Q

what antigen is in matrix

A

m-antigen

163
Q

what antigen is in capsule

A

k-antigen

164
Q

what antigen is in flagella

A

h-antigen

165
Q

what are bacterial serotypes

A

different surface antigens in a bacteria

166
Q

what is hemagglutinin

A

viral fusion with target cells so they can get in

167
Q

what is neuraminidase

A

release of mature viral particles from the host cells so they can get out

168
Q

what is antigenic drift

A

genetic changes that can arise through replication of viral genomes by error-prone nucleic acid polymerases (variant strains)

169
Q

what does antigenic drift lead to

A

changes in the surface molecules of the virus that the immune system cannot recognize

170
Q

what is antigenic shift

A

closely related variants infect the same host cell and mix their genetic components during replication and assembly to create new viral particles with characteristics from both strains

171
Q

what can antigenic shift cause

A

pandemics because the new virus has not been encountered before

172
Q

what are zoonotic pathogens

A

pathogens from animals

173
Q

what are three different mechanisms for genetic variation in pathogens

A
  1. having multiple varied copies of a gene that contain their own on/off switch
  2. having one expression locus with many silent gene copies that be switched into locus via gene rearrangement when necessary
  3. having a highly variable region in a gene product that can change when necessary
174
Q

how does neisseria spp. exhibit antigenic variation

A
  1. uses multiple gene copies of Opa outer membrane protein
  2. express variant of the pilin gene
  3. vary sugars at ends of lipooligosaccharide molecules in their outer membranes
175
Q

what is viral latency

A

viruses are still alive but not actively replicating so they can invade the immune system

176
Q

what are extracellular bacteria targeted by

A

phagocytosis, opsonization, and neutralization via immunoglobulins

177
Q

how do intracellular pathogenic bacteria avoid destruction

A

-survive within the cytosol of the phagocyte and escape the phagosome
-prevent the formation of the phagolysosome
-survive in the phagolysosome without being digested by the phagocyte

178
Q

how is the phagosome escaped

A

use a pore-forming toxin to punch holes in the phagosome membrane

179
Q

how is the fusion of phagosome-lysosome blocked

A

target proteins involved in membrane trafficking and fusion

180
Q

how do pathogens survive in the phagolysosome

A

polysaccharide capsule inhibits reactive oxygen species produced in the lysosome

181
Q

what do bacterial toxins do

A

alter normal immune system behavior or cellular activity

182
Q

what are the two groups of toxins

A

endotoxins (present as a component of the pathogen) and exotoxins (secreted by the pathogen)

183
Q

how do extracellular pathogens disrupt phagocytosis

A

inhibit the actin cytoskeleton needed for phagocytosis

184
Q

how is cytokine signaling disrupted

A

target the expression of cytokines and block the activation of NFkB

185
Q

how does disruption of toll-like receptors affect detection

A

pathogens can persist if tlr’s cannot signal detection

186
Q

how is the complement system disrupted

A

-preventing complement fixation
-precent membrane-attack complex formation

187
Q

how is the adaptive immune system disrupted

A

-subverting mhc1 presentation
-blocking lymphocyte activation or lymphocyte effector mechanisms
-degrading IgA at mucosal surfaces using an enzyme

188
Q

tolerable immunodeficiencies

A

result from mutations that have limited effects in a select number of cells

189
Q

why is a b-cell immunodeficiency most common

A

b-cell immunodeficiencies can be tolerable but t-cell and innate cell immunodeficiencies usually cause severe morbidity

190
Q

sever combined immunodeficiency

A

-scid
-susceptible to infection by many types of microbes
-lack both t and b cells
-results from impaired immune cell development

191
Q

examples of acquired immunodeficiencies

A

-lack of vitamin a in people who are malnourished
-aids caused by hiv

192
Q

how can the first defenses be targeted for increases susceptibility to infections

A

-defects in epithelial barriers and pathogen recognition receptors
-defects in peptides and enzymes that enhance pathogen-fighting activities

193
Q

how can an immunodeficiency of the complement system arise

A

defects in virtually any component of the complement system can result in impaired responses to microbes

194
Q

hereditary angioneurotic edema (hane)

A

-results from mutations in the c1 inhibitor (c1-inh) gene
-C1 is not inhibited by the C1 protease so C2 and C4 do not get cut
-there is too much C2a which is a vasodilator and causes edema

195
Q

neutropenia

A

result of mutations that affect neutrophil development which creates a susceptibility to microbial infections

196
Q

how can phagocyte function be impared

A

lack of specific immune cells or mutations that affect phagocytic pathways
ex) defects in NADH oxidase or proteins related to the oxidative burst

197
Q

leukocyte adhesion deficiency (lad)

A

-due to mutations in the beta-2 integrin that is shared by the LFA-1, CR3, and CR4 adhesion proteins
-loss of LFA-1 impairs innate cell migration to sites of infection
-loss of CR3 and CR4 results in an inability to efficiently recognize C3b on pathogens
-patients are susceptible to recurrent acterial infections

198
Q

chediak-higashi syndrome

A

-autosomal recessive mutation in LYST gene
-LYST protein is normally responsible for formation of phagolysosome
-susceptible to recurring gram+ bacterial infections

199
Q

chronic granulomatous disease

A

-mutations in genes responsible for the function of NADPH oxidase
-nadph oxidase activity results in production of reactive oxygen species and the respiratory burst
-inefficient killing of microbes result in chronic inflammation and formation of granulomas
-susceptible to recurrent bacterial and fungal infections

200
Q

classical nk cell deficiency

A

-results from impaired production of nk cells
-caused by rare mutations in the transcription factor GATA3 or the dna replication protein MCM3

201
Q

functional nk cell deficiency

A

-results from impaired function of nk cells
-caused by rare mutation in the FCyR CD16 gene that is responsible for initiating antibody-dependent cell-mediated cytotoxicity (adcc)

202
Q

adenosine deaminase (ada) deficiency

A

-build up of dATP in developing lymphocytes inhibits cells from completing cell division

203
Q

how are scid patients treated

A

-diagnosis it pre or perinatally so treatment can begin after birth
-bone marrow transplant to restore normal lymphocyte production
-transfer of antibodies from healthy individuals

204
Q

why are t-cell immunodeficiencies so severe

A

t-cells have many function including initiation of immune responses and killing infected cells which results in susceptibility to bacterial, fungal, and viral infections

205
Q

JAK3 deficiency

A

-the y-common chain of cytokine receptors involved in t-cell development and maturation is mutated
-JAK3 signals downstream of the y-common chain so when mutated it cannot signal

206
Q

purine nucleotide phosphorylase (pnp) deficiency

A

-similar to ada deficiency but developing t-cells are mainly affected
-clonal expansion is shut down because dGTP builds up and DNA synthesis is shut down

207
Q

DiGeorge Syndrome

A

-chromosomal translocation resulting in multiple defects in organ development
-lack of a thymus so there is reduced t-cells and susceptibility to many microbial infections

208
Q

bare lymphocyte syndrome (bls)

A

-loss of mhc proteins on the cell surface results in an inability of t-cells to become activated

209
Q

defects in tcr signaling pathways

A

-mutations in CD3 signaling proteins or in ZAP70 can result in both reduced t-cell production and impair t-cell activation
-can also be caused by immunosuppressive drugs that block t-cell signaling pathways

210
Q

x-linked agammaglobulinemia

A

-most common b-cell scid
-due to mutations in Bruton’s tyrosine kinase (BTK)

211
Q

hyper IgM syndrome

A

defects in isotype switching signals or enzymes results in overproduction of IgM isotype antibodies and inefficient switch t other isotypes

212
Q

Selective IgA deficiency

A

-defects in transport of IgA from basal to apical mucosal epithelia
-results in poor neutralization of microbiota and recurrent opportunistic infections
-can also result in asthma due to poor clearance of environmental antigens or autoimmunity

213
Q

human immunodeficiency virus

A

retrovirus with an RNA genome that is packaged while proteins needed for reverse transcription and replication

214
Q

reverse transcriptase

A

converts RNA to DNA

215
Q

integrase

A

integrate cDNA into host genome

216
Q

HIV protease

A

cleaves polypeptides into functional proteins

217
Q

gp120 and gp41

A

binds to CD4 and a co-receptor (either CCR5 or CXCR4)

218
Q

know stuff about HIV and AIDS

A

there were a lot of slides about them

219
Q

hypersensitivity reaction

A

stimulation of an immune response to a harmless foreign material

220
Q

allergies

A

one of the most common type of hypersensitivity reactions
-type 1 hypersensitivity

221
Q

allergens

A

-recognized by the immune system and inflammatory mediators are released
-typically small peptides, proteins, or drugs

222
Q

type 1 hypersensitivity

A

mast cells, eosinophils, and basophils respond to a foreign molecule capable of binding to IgE associated with these granulocytes

223
Q

type 2 hypersensitivity

A

IgG immunoglobulins which recognize cell-surface molecules target cells containing these molecules via the complement pathway or antibody-dependent cell-mediated cytotoxicity

224
Q

type 3 hypersensitivity

A

caused by the action of IgG recognizing soluble antigens and forming immune complexes which results in unnecessary activation of complement and activation of phagocytic cells

225
Q

serum sickness

A

example of type 3 hypersensitivity

226
Q

type 4 hypersensitivity

A

caused by the delayed activation of t cells by a foreign, harmless antigen

227
Q

delayed-type hypersensitivity

A

-when the type 4 hypersensitivity response is induced
-dictated by the type of t cells that are activated

228
Q

examples of inflammatory mediators

A

histamine, leukotrienes, prostaglandins, heparin

229
Q

what is the hygiene hypothesis

A

“kids don’t eat enough dirt”
increases in allergies in developed countries may be due to lack of exposure to microorganisms

230
Q

how do granulocytes mediate hypersensitivity

A

granulocytes have Fc receptors specific for IgE (Fcepsilon) that allergens bind to

231
Q

how do mast cells contribute to type 1 hypersensitivity

A

mast cells in conjugation with IgE release inflammatory mediators from cytosolic granules when they recognize pathogens which causes allergic responses from rhinitis to anaphylaxis

232
Q

how are basophils involved in type 1 hypersensitivity

A

basophil degranulation is activated similarly to mast cell degranulation when antigens are recognized via associated IgE

233
Q

how are eosinophils involved in type 1 hypersensitivity

A

IgE signaling causes eosinophils to secrete proteins such as inflammatory mediators (histamine and prostaglandins) and toxic molecules

234
Q

what are routes of entry for an allergen and how severe are they

A

less severe: skin contact, inhalation
more severe: ingestion, injection

235
Q

how does exposure to an allergen lead to an allergic reaction

A

-an individual is sensitized by first exposure to the antigen which elicited the primary adaptive immune response
-allergen-specific t and b cells and IgE that binds to granulocytes are produced
-second exposure to the allergen causes an allergic reaction

236
Q

wheal-and-flare reaction

A

a small amount of allergen is injected and results in a raised skin lesion containing fluid (wheal) surrounded by a red, itchy area (flare)

237
Q

urticaria

A

-skin reaction
-hives
-itchy, red welts on the skin

238
Q

what is anaphylaxis

A

a widespread activation of blood-vessel-associated mast cells in the body caused by allergens in the blood stream that results in body-wide vasodilation

239
Q

atopic

A

individuals with an increased predisposition to type 1 hypersensitivity and express more IgE that are capable or recognizing innocuous allergens

240
Q

what are some treatments for allergy symptoms

A

-corticosteroids used in topical creams and oral/inhaled forms to suppress the action of inflammatory mediators
-immunotherapy with oral or injection administration of allergens to desensitize the individual

241
Q

what are examples of IgM and IgG activity in type 2 hypersensitivity reactions

A

-opsonization in phagocytosis
-activation of complement on recognized cells
-activation of antibody-dependent cell-mediated cytotoxicity

242
Q

antibody-dependent cell-mediated cytotoxicity

A

using the FcgammaRIII receptor, NK cells recognized bound IgG and target the cell by releasing cytotoxic molecules and inducing apoptosis

243
Q

what is the result in a type 2 hypersensitivity reaction

A

-destruction of the cell through phagocytosis
-lysis through action of MAC
-destruction by NK cells

244
Q

how can transfusion of incompatible blood produce a type 2 hypersensitivity reaction

A

immunoglobulins to certain blood type glycolipid antigens can mark blood cells bearing those glycolipids as ‘foreign’

245
Q

type o blood

A

have H antigen glycolipids and do not have glycosyltransferases that can modify H antigen

246
Q

type a blood

A

express glycosyltransferase that adds the carbohydrate n-acetylgalactosamine to h antigen

247
Q

type b blood

A

express glycosyltransferase that adds the carbohydrate galactose the h antigen lipid

248
Q

type ab blood

A

express both glycotransferases and can make both a and b antigen glycolipids

249
Q

what rhesus factor is most important

A

Rh D antigen

250
Q

what does it mean to have a positive blood type

A

the individual is positive for the Rh D antigen

251
Q

hemolytic disease of the newborn

A

-a type 2 reaction that occurs during pregnancy when an Rhneg mother conceives an Rhpos fetus after giving birth to an Rhpos child
-Rh-specific IgG production results in destruction of fetal RBCs resulting in severe anemia or death of the developing fetus

252
Q

crossmatching

A

checks for harmful interactions between a potential donor and recipient of blood, tissue, or an organ

253
Q

what occurs in a type 3 hypersensitivity reaction

A

IgM and IgG recognize soluble antigens and prompt the formation of immune complexes and inefficient clearance results in abnormal activation of inflammatory responses and cells that attempt to clear the immune complexes

254
Q

what factors influence if immune complexes can drive a type 3 hypersensitivity reaction

A

-the affinity of a particular antigen to a specific location or tissue
-disruption of normal phagocytosis
-the chemical nature of the antigen which plays a role in how efficient phagocytic cells are at engulfing the antigen

255
Q

serum sickness

A

type 3 hypersensitivity reaction

256
Q

arthus reaction

A

type 3 hypersensitivity reaction that occurs when large amounts of antigen are deposited and immune complexes form

257
Q

what are the phases of type 4 hypersensitivity reactions

A

sensitization phase and effector phase

258
Q

what is required for a type 4 hypersensitivity reaction

A

antigen-presenting cells to present to t cells

259
Q

what happens in the sensitization phase of a type 4 hypersensitivity reaction

A

APCs present antigen to T cells via mhc molecules to activate the t cell bearing the receptor that can recognize the mhc antigen complex

260
Q

what happens in the effector phase of type 4 hypersensitivity reaction

A

-a subsequent exposure to the sensitized t cell drives differentiation of the t cell into an effector t cell
-the t cell activated is usually a TH1 helper t cell, which secretes IFN-y and CXCL8, activating and recruiting macrophages

261
Q

how are type 4 hypersensitivity reactions induced

A

intracellular bacteria, viruses, fungi, and chemicals

Immunology Quiz Questions (15 decks)

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