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Immunology > Part 1 > Flashcards

Part 1 Flashcards

1
Q

what is the first line of defense

A

innate immune system: skin and mucous membranes

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2
Q

what is the innate immune system

A

the defenses you are born with

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3
Q

what is the innate immune system made up of

A

Surface barriers:
Skin
Mucous membranes

Internal defenses:
Phagocytes
Fever
NK cells
Antimicrobial proteins
Inflammation

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4
Q

what is the second line of defense

A

Internal defenses:
Phagocytes
Fever
NK cells
Antimicrobial proteins
Inflammation

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5
Q

what is the third line of defense

A

adaptive immunity

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6
Q

what is adaptive immunity

A

immunity that is built up over time

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7
Q

what are the parts of the adaptive immunity

A

lymphocytes (B and T), antibodies, antigen presenting cells (macrophages and dendritic cells)

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8
Q

what are the roles of the third line

A

Recognizes specific foreign substances
Acts to immobilize, neutralize, or destroy foreign substances
Amplifies inflammatory response and activates complement.

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9
Q

what is humoral immunity

A

the process of adaptive immunity manifested by the production of antibodies by B lymphocytes. It develops in bone marrow. B cells may be triggered to proliferate into plasma cells. Plasma cells produce antibodies.

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10
Q

what do B cells do

A

protect you from infection by making proteins called antibodies.

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11
Q

what are B cells

A

B-cells are a type of white blood cell called lymphocytes. When your immune system detects antigens — markers that indicate a threat like a bacteria or virus has entered your body — your B-cells produce antibodies to fight the invader.

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12
Q

what are T cells

A

a type of white blood cell called lymphocytes.
Cytotoxic T-cells destroy infected cells. Helper T-cells send signals that direct other immune cells to fight infection.

wipe out infected or cancerous cells. They also direct the immune response by helping B lymphocytes to eliminate invading pathogens.

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13
Q

do plants and bacteria have immune systems

A

yes

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14
Q

what is the plant immune system made up of

A

The cuticle (barrier).
Phytoalexins: low molecular weight antimicrobial compounds that are produced by plants as a response to biotic and abiotic stresses. As such they take part in an intricate defense system which enables plants to control invading microorganisms.

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15
Q

what is the bacteria immune system made up of

A

Endonucleases (Restriction Enzymes): recognizes and cleaves foreign DNA on the defined recognition sites.
Chopped up virus DNA is later re-inserted into the bacterial genome so the bacteria can remember the virus.

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16
Q

what are the three categories of the immune system anatomy

A

lymphatic vessels, lymphatic organs, and lymph fluid

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17
Q

what do the lymphatic vessels do

A

regulate fluid homeostasis, assist in immune surveillance, and transport dietary lipids.
Anastomosis: coming together after being branched off.

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18
Q

what are the lymphatic organs

A

Lymph nodes
Spleen
Appendix
Peyer’s patches (tissue)
Thymus
Bone marrow

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19
Q

what is lymph

A

the fluid that flows through the lymphatic system

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20
Q

what is the function of lymph

A

carries the waste products and destroyed bacteria back into the bloodstream. The liver or kidneys then remove these from the blood. The body passes them out with other body waste.

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21
Q

what is interstitial fluid

A

plasma that is leaked out of the blood capillaries

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22
Q

what is the difference between plasma and interstitial fluid

A

plasma resides in blood vessel
IF resides outside of the blood vessel

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23
Q

what is IF made up of

A

containing sugars, salts, fatty acids, amino acids, coenzymes, hormones, neurotransmitters, white blood cells and cell waste-products.

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24
Q

what is the hierarchy of the lymph system

A

Lymph capillaries > lymph vessels > lymph trunk > lymph ducts.

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25
Q

what do monocytes mature to

A

macrophages, which differentiate in tissues

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26
Q

what cells are in the second line of defense

A

macrophages, neutrophils, basophils, eosinophils, NKs, and ILCs 1-3

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27
Q

what antimicrobial proteins are in the second line

A

complement, defensins, cathelicidins, histatins, interferons (A, B, G), lysozyme, and phospholipase A2

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28
Q

do lymph capillaries have valves?

A

yes

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29
Q

what are afferent vessels

A

vessels that go into the node

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30
Q

what are efferent vessels

A

vessels that go out of the node

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31
Q

what is the medulla

A

most inner portion of LN

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32
Q

what is the cortex

A

outer portion of the inside of the lymph node.
Contains follicle and germinal center.

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33
Q

what is the follicle

A

a loosely arranged structure with an outer mantle of small T lymphocytes and agerminal center composed of B lymphocytes, follicular dendritic cells, and macrophages.

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34
Q

what is the germinal center

A

in the follicle, attached to paracortical zone (T cells)
producing long-lived antibodies secreting plasma cells and memory B cells (activated), which can provide protection against reinfection.
T cells outside of the germinal center continuously activate B cells.

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35
Q

what types of pulp are in the spleen

A

red and white

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36
Q

what does white pulp do

A

produces WBCs

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37
Q

what does red pulp do

A

produce RBCs

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38
Q

where are Peyer’s patches located

A

intestines

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39
Q

what do Peyer’s patches do

A

samples stomach contents for invaders

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40
Q

where is the thymus

A

near the heart

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41
Q

what does the thymus do

A

where T cells develop
Doesn’t stop growing until puberty, then atrophies as you get older.
Secretes thymosin and thymopoietin that causes T lymphocytes to become immunocompetent.

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42
Q

what are the three types of pathogens

A

bacteria, viruses, parasites

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43
Q

how does bacteria enter the body

A

through direct bodily contact, open wounds, inhalation, or ingestion.

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44
Q

what are the properties of viruses

A

nucleic acids enclosed in protein coats. Some are enclosed by a membrane.
Most infect hosts to replicate.
May kill the host rapidly or lie dormant.
May cause cancer.
Must enter the cell to cause harm.

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45
Q

types of parasites

A

protists, fungi, worms

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46
Q

properties of parasites

A

Damage the host by using host nutrients or secreting toxic chemicals.

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47
Q

what are extracellular pathogens

A

cytoplasm-based
Bacteria (some are intracellular)
Parasites.

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48
Q

what are intracellular pathogens

A

vesicle-based
Viruses
Some bacteria

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49
Q

what are the other 3 subcategories for pathogens

A

epithelial, blood, IF

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50
Q

what are the properties of the skin

A

Keratin
Dryness, sebum, pH (pH between 3 and 4)
Normal microbiota
S. epidermidis

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51
Q

properties of GI tract

A

pH of 1 to 2
Vomiting cleans out any pathogens.

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52
Q

properties of resp tract

A

Trachea has cilia, goblet cells, and mucus to trap invaders.
Has antibodies

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53
Q

properties of the genitourinary tract

A

Urination cleans out bacteria in the tract.

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54
Q

properties of the eyes

A

Lacrimal glands help wash eyes from bacteria.
Tears have lysozyme and antibodies.

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55
Q

properties of sweat

A

Sweat has lysozyme and phospholipase A2 in body secretions.
Very salty environment.

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56
Q

how does lysozyme kill

A

Lysozyme is an enzyme that degrades glycosidic bonds between NAG and NAM in cell walls

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57
Q

how does phospholipase A2 kill

A

hydrolyzes phospholipids in membranes

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58
Q

what are granulocytes

A

neutrophil, baso, eosino

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59
Q

what are the big three phagocytic cells

A

neutro, macro, and dendritic

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60
Q

what are ILCs and NKs homologs to

A

T cells

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61
Q

what are NKs similar to

A

CD8 T cells

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62
Q

what are ILCs similar to

A

CD4 T cells

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63
Q

what does inflammation and fever cause

A

Inflammation causes neutrophils, macrophages, and dendritic cells to migrate to the site of infection.
Also brings nutrients to repair damaged tissue.
Brings antimicrobial proteins
After lymph is leaked, the mix of lymph and phagocytic and dendritic cells are drained into the lymph vessel.
When these cells go to the lymph node, they are met with T and B cells)

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64
Q

what are the characteristics of inflammation

A

heat, redness, swelling, pain

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65
Q

what cell gives rise to all blood cells

A

pluripotent hematopoietic stem cells (PHSC)

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66
Q

heirarchy of T, B, and NK cells

A

PHSC >
common lymphoid progenitor>
B/T/NK cell>
B/T/NK cell moves to LN>
B/T/NK cell activated

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67
Q

heirarchy of dendritic cell

A

PHSC >
common myeloid progenitor >
immature DC >
DC moves to tissues >
DC matures in LN

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68
Q

heirarchy of granulocytes

A

PHSC >
common myeloid progenitor >
gran/macro progenitor (blood) >
neutro/baso/eosino

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69
Q

heirarchy of mast and macros

A

PHSC >
common myeloid progenitor >
monocyte or mast cell precursor (blood) >
mature mast or macro (tissues)

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70
Q

properties of macrophages

A

3-8% of cells
Eats everything, including cancer cells.
Microglial: CNS
Kupffer cells (liver)
Alveoli (lungs)

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71
Q

properties of neutros

A

60-70%
Eat bacteria.
Die soon after they consume bacteria
What pus is made of
MO clean out dead neutrophils

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72
Q

properties of basophils

A

0.5%-1%
Promotion of allergic responses and augmentation of anti-parasitic immunity.

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73
Q

percentage of eosinos cells

A

2-4%

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74
Q

what are the most important phagocytic cells

A

macros and neutros

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75
Q

which granulos relate most to parasitic

A

baso and eosino

76
Q

how do baso and eosino kill parasites

A

The granules in these cells contain various cytotoxic granule proteins and reactive oxygen species that can be released to kill parasites (death by a thousand cuts)

77
Q

what do mast cells release

A

granules containing histamine and active agents

78
Q

what are pattern recognition receptors

A

a class of receptors that can directly recognize the specific molecular structures on the surface of pathogens, apoptotic host cells, and damaged senescent cells.

79
Q

where are PRRs found

A

on the surface of macrophages, neutrophils, and dendritic cells
Also in GI and Resp lining cells

80
Q

what do PRRs recognize

A

recognize Pathogen-associated molecular pattern molecules (PAMPs)

81
Q

what are PAMPs

A

a diverse set of microbial molecules that share a number of different general “patterns,” or structures, that alert immune cells to destroy intruding pathogens.

82
Q

where are PAMPs located on the antigen

A

on the surface

83
Q

what microorganisms bear PAMPs

A

bacteria, viruses, fungi

84
Q

What are Toll-Like Receptors (TLRs)

A

recognize specific classes of
infecting microbes

85
Q

what do TLRs do if they detect a pathogen (activated)

A

trigger the release of cytokines that support inflammation.

86
Q

what PAMP is on Gram negative bacteria

A

LPS

87
Q

what PAMP is on Gram positive bacteria

A

teichoic acids

88
Q

what receptor binds to recognize fungi

A

mannose receptor

89
Q

what TLRs are always bound together

A

TLR 1 and 2

90
Q

what does TLR 4 do

A

leads to the production of pro-inflammatory cytokines via the MyD88 dependent or independent pathway.

91
Q

what do scavenger receptors do

A

recognize anionic charges

92
Q

what is the first step of when bacteria bind to receptors

A

they are engulfed and degraded by lysosomes.

93
Q

what is the second step of when bacteria bind to receptors

A

Bacteria components are bound to receptors that trigger transcription of inflammatory cytokines. Cytokines are released into bloodstream.

94
Q

what happens when cytokines are released into bloodstream

A

blood vessels swell due to relaxed smooth muscle in the vessel. This loosens the junctions of vessel cells. Interstitial fluid leaks more into the cells.

95
Q

what is also released when macrophages are triggered by bacteria

A

chemokines

96
Q

what do chemokines do

A

induce cell migration

97
Q

what is extravasation

A

white blood cells travel through blood cell walls and tissues to locate and manage injuries and infections.

98
Q

what is the first step of extravasation

A

rolling adhesion

99
Q

what is the function of rolling adhesion

A

selectins are on epithelial/leukocyte/platelet cells, which bind loosely to neutrophils, which slows down cells

100
Q

second step of extravasation

A

Tight binding: ICAM (intracellular adhesion molecule) tightly bind to neutrophil

101
Q

third step of extravasation

A

Diapedesis: move WBC through blood capillary cell walls

102
Q

fourth step of extravasation

A

Migration: neutrophil fully moves from capillary to tissue

103
Q

what does plasma contain

A

sugars, salts, buffers, wastes, oxygen, CO2, proteins (albumin 60%) (globular alpha, beta, gamma (antibodies) 36%) (fibrinogen 4%).

104
Q

what is the complement system

A

made up of a large number of distinct plasma proteins that react with one another to opsonize pathogens and induce a series of inflammatory responses that help to fight infection.

105
Q

how many proteins are in the complement system

A

about 30

106
Q

what do the proteins in the complement system react with

A

PAMPs

107
Q

what do the majority of the proteins in the complement systems do

A

A number of complement proteins are proteases that are themselves activated by proteolytic cleavage.

108
Q

how is the classical complement system activated

A

by antibody-antigen binding on bacterial surfaces

109
Q

classical complement pathway

A

antigen-antibody contact cause conformational changes >
C1 >
C2 and C4 > cleavage of both components
C2a and C4b converge >
C3 formed > cleaved
C3b and C3a

110
Q

what does C3b result in (all)

A

opsonization and cytolysis

111
Q

what does C3a result in (all)

A

inflammation

112
Q

what is opsonization

A

an immune process which uses opsonins to tag foreign pathogens for elimination by phagocytes.

113
Q

how is alternative complement system activated

A

triggered by contact with various proteins, lipids and carbohydrate structures on microorganisms and other foreign surfaces

114
Q

alternative complement pathway

A

B, D, and P factors bind to microbe’s lipid-carb complexes >
C3 > cleaved
C3b and C3a

115
Q

how is lectin complement system activated

A

lectin binds to the microbe’s surface carbohydrate, which contains mannose

116
Q

what is the lectin complement system pathway

A

lectin binds to microbe’s surface carb (mannose) >
C2 and C4 > cleaved
C2a and C4b converge >
C3 >
C3b and C3a

117
Q

what are interferons

A

a group of signaling proteins made and released by host cells in response to the presence of viruses, bacteria, parasites or tumor cells. .

118
Q

what is the function of interfeons

A

allow for communication between cells to trigger the protective defenses of the immune system that eradicate pathogens or tumors.

119
Q

what happens when interferons are transcripted

A

interferons are released from the cell, which bind to neighboring cells. Neighboring cells transcribe and release antiviral peptides (AVPs) that degrade viral mRNA

120
Q

what do IFNs cause

A

Inflammation
Cell replication/activation
Production of AVP
Production of other cytokines
chemotaxis

121
Q

what do alpha and beta IFNs do

A

Cause cells to produce
antiviral proteins that
inhibit viral replication

122
Q

what do gamma IFNs do

A

Causes
neutrophils and
macrophages
to phagocytize bacteria.

123
Q

what does virulent mean

A

ability of an organism to infect the host and cause a disease.

124
Q

how can pathogen virulence vary

A

If the pathogen:
Has a capsule that helps evade the immune system.
Has toxins that are released and kill cells
Enzymes that are secreted that evade immune system
The number of pathogens that dictates whether or not you get sick.

125
Q

how does number of pathogens determine virulence

A

Sufficient numbers of pathogen overwhelm second line of defense (phagocytic cells)

126
Q

what happens when a pathogen gets degraded

A

a vesicle with a receptor binds to the degraded pathogen and is later expressed on the cell surface of the phagocytic cell. MHC II is what is expressed on the cell surface.

127
Q

what is an antigen

A

a fragment of the pathogen that triggers an immune response.

128
Q

what happens after an antigen is expressed on MHC II

A

Antigen–MHC complexes are recognized on the cell surface by the TCR of CD4+ T cells

129
Q

what cell only recognizes proteins

A

T cells

130
Q

what are antigen presenting cells

A

phagocytic cells

131
Q

what is TH1

A

T Helper cell 1

132
Q

what do TH1s produce

A

interferon-gamma, interleukin (IL)-2, and tumour necrosis factor (TNF)-beta

133
Q

what do TH1 products do

A

activate macrophages, NKs, and CD8s

134
Q

what do TH1s determine

A

whether pathogen is viral or bacterial

135
Q

what do TH1s mainly fight

A

any intracellular pathogen

136
Q

what do TH2s mainly respond to

A

pathogens in mucus or parasites

137
Q

what do TH17s mainly respond to

A

anything extracellular

138
Q

what do TH17s activate

A

neutrophils

139
Q

what is the purpose of THs

A

they are T regulatory cells

140
Q

what do TH2 cells activate

A

baso, eosino, Mast

141
Q

when are NKs and CD8s activated

A

during a virus or when a cell is stressed (cancer)

142
Q

how do NKs destroy cells

A

by releasing of lytic granules or by inducing death receptor-mediated apoptosis

143
Q

how do CD8s destroy

A

by releasing granzymes and perforin (causes holes in membrane)

144
Q

what do dendritic cells activate

A

CD4, CD8, NKs, B cells.
DCs do not fully activate CD8/NK

145
Q

what are the regions of antibodies

A

variable and constant region

146
Q

what is the variable region

A

top part of the Y
unique and created at random

147
Q

what is the function of the variable region

A

The primary role of the antibody variable region is to bind to the target antigen.

148
Q

what is the constant region

A

bottom part of the Y
always is the same

149
Q

what is the function of the constant region

A

determines the mechanism used to destroy antigen

150
Q

where do T cells come from

A

bone marrow to thymus (mature)

151
Q

where do B cells come from

A

red bone marrow

152
Q

how are T cells selected in the thymus

A

Thymic cells present a self-antigen to t cell receptor, and bind.

153
Q

what is positive selection if cell fails to recognize self-MHC

A

apoptosis; binds too loose.

154
Q

what is positive selection if it binds to MHC correctly

A

causes MHC restriction of survivors; bound at correct tightness and leave thymus.

155
Q

what is negative selection if T cells bind to MHC and reacts vigorously with self-Ag

A

causes apoptosis, which causes surviving cells to become self-tolerant; too tight of binding, and might cause mounting in immune response when it doesn’t need to.

156
Q

what is the postulates of clonal selection theory

A

in a preexisting group or population of lymphocytes, a particular antigen can activate only its specific counter cell, inducing that specific cell to multiply and create clones for antibody production

157
Q

where does the removal of potentially immature lymphocytes by clonal deletion happen

A

thymus

158
Q

where does differentiation happen for T cells

A

thymus

159
Q

where does the pool of mature naive lymphocytes

A

thymus

160
Q

what is peripheral immunocompetence

A

immunological tolerance developed after autoreactive T and B cells mature and enter the periphery.

161
Q

where does the proliferation and differentiation of activated specific lymphocytes to form a clone of effector cells happen

A

peripheral

162
Q

stages of antigen presenting

A

B cell presents antigen to T cell >
T cell sends signals >
T cell diff into TH1 or 2

163
Q

what is the role of MHCII

A

to present processed antigens, which are derived primarily from exogenous sources, to CD4(+) T-lymphocytes. MHC class II molecules thereby are critical for the initiation of the antigen-specific immune response.

164
Q

what is the role of MHCI

A

to display intracellular proteins to cytotoxic T cells (CTLs). However, class I MHC can also present peptides generated from exogenous proteins, in a process known as cross-presentation.

165
Q

what do T cells recognize

A

proteins only

166
Q

what is the role of BCRs

A

interacts with foreign antigens to mediate B cell activation and secretion of antibodies.

167
Q

how many TCRs are there

A

about 100,000

168
Q

how many TCRs need to be bound to create activation

A

50

169
Q

what is clonal selection

A

picking the specific T cell to the antigen.

170
Q

what is clonal expansion

A

army created of the specific T cell.

171
Q

what is clonal differentiation

A

maturation of the naive T cell.

172
Q

what are TH and T cells complements of

A

ILCs

173
Q

what are NKs complement to

A

CD8 T cells

174
Q

why is MHC I expressed

A

it is a way for infected cells to express to the immune system that it needs CD8 cells through expressed pathogen particles on the cell surface.

175
Q

what do plasma cells secrete

A

antibodies

176
Q

how does the antibody bind to an antigen

A

Antibody can bind directly to the antigen; antigen does not need to be digested first.

177
Q

how does a antibody react to an antigen

A

neutralization or opsonization

178
Q

Describe how the second and third branches of immune system are interlinked and
help/regulate each other

A

The innate immune system tells the adaptive immune system when it’s time to help mount a defense.
The phagocyte is also known as an antigen-presenting cell because after engulfing the invading microbe, it displays pieces of protein from the microbe, called antigens, on its surface, on what is known as the major histocompatibility complex (MHC) molecule. This alerts the adaptive immune system and allows cells known as T cells to recognize an infected cell.

179
Q

effector functions of CD4

A

crucial in achieving a regulated effective immune response to pathogens. Naive CD4⁺T cells are activated after interaction with antigen-MHC complex and differentiate into specific subtypes depending mainly on the cytokine

180
Q

effector function of CD8 cells

A

kill virus-infected cells and produce antiviral cytokines such as interferon gamma. In this way, CD8 T lymphocytes contribute to resisting primary and secondary viral infections.

181
Q

effector functions of antibodies

A

Antibodies are secreted into the blood and mucosa, where they bind to and inactivate foreign substances such as pathogens and toxins (neutralization).
Antibodies activate the complement system to destroy bacterial cells by lysis

182
Q

what is positive in t cells

A

T cells in the thymus that bind moderately to MHC complexes receive survival signals, which turn T cells into mature, specific t cells.

183
Q

what is negative selection in t cells

A

deletes T cells with high affinity for self-peptides via apoptosis, thus ensuring selftolerance, and is presumed to reflect strong signaling via TCR recognition of peptide–MHC complexes on APC.

184
Q

what is positive selection in b cells

A

Developing B cells are positively selected when the pre-B receptor binds its ligand.

185
Q

what is negative selection in b cells

A

binding to the receptor results in cell death ( self tolerance)

Immunology (11 decks)

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