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BIO233 > Immune system > Flashcards

Immune system Flashcards

1
Q

What is blood made up of

A

liquid (plasma) and cellular (red and white) component

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2
Q

Where does blood come from

A

Blood cells arise from Hematopoietic stems cells in the bone marrow.
Myeloid stems cells and Lymphoid stem cells

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3
Q

What are the two types of stem cells

A

Myeloid stem cells and lymphoid stem cells

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4
Q

Adaptive immunity

A

Also called acquired or specific immunity
Develops after exposure to pathogens or antigens
Slow and specific response

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5
Q

Innate immunity

A

Present in all animals before exposure to pathogens
Involveds FIRST and SECOND lines of defense
Fast and nonspecific response to infection
External barriers, internal cellular, and chemical defenses

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6
Q

First line of defense (physical)

A

Skin: Tightly packed cells of outer epidemris (+keratin = tough protein preventing entry of m/o)

Mucous membranes: Lines GI, GU, and resp

Ciliary escalator: trapped and transport microbes away from lungs

Washing action: tears, salvia, urine, and vaginal secretions

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7
Q

Chemical factors of first line of defenese

A

Secretions: Skin pH 3-5 (inhibits microbes bc most are neutrophils)

Lysozyme: enzyme in skin, saliva, and tear secretions
Degrade peptidoglycan layer of bacteria making them susceptible to lysis

Fungistatic fatty acid in sebum
Lactic acid in V

Produce lactic acid (acidic pH)
Stomach acid is lethal to most bacteria

Normal microflora: Antoagism/competiic
Some are opportunistic pathogens

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8
Q

Lysozyme

A

enzyme in skin, saliva, and tear secretions
Degrade peptidoglycan layer of bacteria making them susceptible to lysis

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9
Q

4 second line of defenses

A

Defensive cells
Inflammation
Fever
Antimicrobial substances

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10
Q

What are the defense cells of the body

A

WBCs (leukocytes) engulf pathogens via phagocytosis

Phagocytic cells

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11
Q

What types of phagolytic cells are there

A

Macrophages: ciricrulating phagocytes
Neutrophils: Stimulate acquired immunity
Dendtricic cells: stimulate acquired immunity

Engulf and destroy pathogens
Act as antigen presenting cells

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12
Q

How does phagocytosis occur

A

Chemotaxis and adherence of m/o tophagocyte
Ingestion of m/o to form phagosome
Phagolysome: Fusion b/ww phagosome and lysosome (ingested m/o digested by enzymes)
Residual body containing indigestible material that are discharged as waste to outside
Some m/o pieces presented on surace of APCs

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13
Q

Phagosome

A

a vesicle (encolosure surrounded by a membrane)
Pathogen is swallowed an enclosed in a membrane
Recognized by lysosome

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14
Q

What do phagocytes use tentacles for

A

To grab on to phagosome

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15
Q

How can m/os avoid phagocytosis

A

Capsule preventing adhereance to macrophage
Leukocidins kill macrophage
Lysis of phagolosome
Escape from phagosome
Orevt fusion of phagosome with lysosome
Survive phagolusosome

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16
Q

How would a m/o lyse the phagosome

A

An organism like Lysteria: Releases enzymes to destroy phagolysosome complex

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17
Q

How does a m/o escape from the phagosome

A

(into the cytoplasm of phagocyte)
i.e Shigella
Begins multiplying inside phagocyte (without worry abt being captured again

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18
Q

How do m/o prevent fusion of phagoosome with lysosome

A

HIV and M. TB
Produces chemicals preventing lysosome from fusing (organism cannot be destroyed)

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19
Q

How do organisms survive phagolysosome

A

Coxiella bunetti (spore) loves it in the phagolysosome
Uses phagosomatic enzyme to activate multiplication process
Eventually break out via phagolysis

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20
Q

Two types of inflammation

A

local
systemic

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21
Q

SS of local inflammarion

A

Redness
Pain
Heat
Swelling (edema)
Loss of function

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22
Q

Steps of inflammation

A

Injury
Mast cells recognize presence of foreign objects, release histamines in response
Histamines cause vasodialation
Skin appears red with increased bloodflow
Vasodialation also brings neutrophils and other cells
Margination: Neutrophils, macrophages (any cells helping in the process of healing) begin sticking to the walls of capillaries
Vasodialtion cause the capillaries to become leaky (fluids ooze out causing edema/swelling) some cells begin to squeeze out of capillaries = emmigration
Macrophages (phagocytes) in the area where bacteria/pathogens are and they begin phagocytosis
In the process, some macrophages die = pus
Neutrophils (also involved in phagocytosis similar to WBCs)
Histamine: released by mast cells
Tissue repair: Occurs by way of chemicals (platelts ) brought by vasodialaiton

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23
Q

Why does warmth occur with inflammation

A

with vasodialtion, as blood brings skin closer to body temperature

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24
Q

What causes pain in inflammaiton

A

Swelling pressing against pain receptors

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25
Q

What is fever

A

A systemic response (a kind of systemic inflammation)
Abnormally high body temp

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26
Q

What are included in internal antimicrobial substances

A

COmplement systems
Interferons
Defensisn

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27
Q

Complement systmes

A

special proteins that attack and lyse microbes

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28
Q

Interfereons

A

proteins secreted by virus infected cells that inhibit viral multiplication in response to viral infection

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29
Q

Defensins

A

proteins secretedby activated mactophags to destroy pathogens to start the process of destroying pathogens

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30
Q

What part of a bacteria causes fevers?

A

Endotoxins

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31
Q

3 ways that complement proteins are involved in the immune response

A

Opsinization
Cytolisis
Activation inflammation

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32
Q

Opsinization

A

Bacteria are marked to be easily reconizable to macrophages (complement protein attached to pathogen)

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33
Q

Cytolisis

A

Breaking up of the bacteria cell (complement proteins have invaded into the membrane of the pathogen)

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34
Q

How do complement proteins aid in the activitation of inflammation

A

Complement protein that attaches to the mast cell that stimulates the mast cell to release histamines that lead to vasodialtion
Aid the body to stimulate inflammation (especially local)

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35
Q

Margination

A

Phagocytes sticking to the walls of blood vessels is a condition known as _________________.

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36
Q

Diapedesis or emigration

A

Fluid and cells leaving the capillaries

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37
Q

Opsinization increases a phagoycites

A

Adherence

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38
Q

Which cell is inbolbed in producing cytokines to activate other immune system cells

A

T cells

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39
Q

leukocidins

A

Molecules that are capable of destroying phagocytes

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40
Q

Measles viruses are capable of inactivating host defenses by

A

suppressing the immune system.
via suppressing activity of cytokines or reproducing within T cells

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41
Q

How are complement proteins labelled

A

With a C and a number 1-9

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42
Q

What are the general requirements for any organism to cause a disease within a host

A

Gaining access to host (portal of entry)
Evasion of host defenses
Adherence to host tissues

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43
Q

Why does V. chloreae have such a high ID50 (10 to the 8)?

A

To cause infection, V. cholerae must survive immune responses AND acidic environment of stomach

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44
Q

What are the properties of exotoxins

A

Target speciic cellular structures or molecules
Protein molecules
Very small amount of exotoxin is lethal

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45
Q

Why are antibiotics alone not ideal treatment for V. cholerae

A

Antibiotic therapy addresses only the growth of V. cholerae; it doesn’t address the extreme dehydration suffered by a person infected with V. cholerae.

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46
Q

What are toxoids?

A

Bacterial exotoxins can be altered to create toxoids, which can be used to produce protective immunity in a host.

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47
Q

Must all pathogens penetrate the body to cause disease?

A

No

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48
Q

Properties of exotoxins

A

Produced and secreted by active/growing cells

Usually inactivated by cooking

Host responds with specific antibodies called antitoxins

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49
Q

Antitoxin

A

Host responds to the production of exotoxins with specific antibodies called antitoxins

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50
Q

Are exo or endotoxins more toxic in smaller doses?

A

Exo

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51
Q

What type of toxins can BOTH G+ and G- produce?

A

Exotoxins

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52
Q

Examples of exotoxins

A

Tetanus toxin
Cholera toxin
Staphylococcal enterotoxin

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53
Q

Properties of endotoxins

A

Produced by Gram-

Released upon phagocytosis/death of cell

May survive sterilization and contaminate medical devices/medications even if completely free of bacteria

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54
Q

Examples of endotoxin using diseasse

A

Salmonella typhi (causing typhoid fever)
Neisseria meningitdis

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55
Q

Do viruses produce endo or exotoxins

A

No

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56
Q

Steps of the A-B exotoxin

A
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57
Q

How can action of A-B Toxin be blocked?

A

Blocking binding sites on B portion of toxin

Inhibiting secretion of proteins from bacterial cell
Blocking receptor mediated endocytosis in cells targeted by A-B toxin
Block host cell receptors to which toxin binds
Block separation of A and B components of toxin

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58
Q

Strategies to block/reduce effects of superantigen toxins

A

Block secretion of proteins by bacterial cells
Block release of cytokines from T cells
Block molecular determinants on superantigens that interact with T cells
Neutralize circulating cytokines

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59
Q

Methods that toxin likely disrupts [plasma membrane of host cell

A

Insertion of protein channel
Disruption of phospholipid bilayer

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60
Q

Possible symptoms of endotoxins

A

Fever, chillls, weakness, fatigue

May worsen after treatment of G- infection

Causing life-threating drop in BP called endotoxin shock

61
Q

Pyrogenic response

A

Fever

62
Q

How does G- bacteria cause fever

A

First, a gram-negative microbe is phagocytized and digested. In the process, endotoxin is released within the phagocytes;

the phagocyte responds by releasing cytokines,

These cytokines are distributed throughout the body by the circulatory system.

When they reach the brain, the hypothalamus responds by releasing prostaglandins, which ultimately raises the body’s temperature and causes a fever.

63
Q

Is a parental route a portal of entry or exit?

A

Both

64
Q

Injections, surgery and deep wounds are examples of what kind of portal of entry?

A

Parental route

65
Q

What kind of anthrax infection is the easiest to acquire

A

Cutaneous antrhax

66
Q

Antigenetic variation

A

process allows pathogens to alter their surface antigens to avoid attack by antibodies produced by the immune system.

67
Q

Invasins

A

These microbial surface proteins rearrange the host cell’s actin filaments, allowing pathogens to enter and move in and between cells.

68
Q

Siderophores

A

proteins that extract iron from host proteins; the bacteria obtain the iron by retrieving these proteins.

By tightly binding iron, removing it from host proteins.

69
Q

nutrient depletion, accumulation of waste products, pathogen entry and exit, and ruptured host cells are examples of what kind of damage?

A

Direct

70
Q

Cytopathic effects

A

These describe the visible effects of viral infections that results in host cell damage.

71
Q

Why does S. aureus need iron

A

Without iron, S. aureus cannot generate energy via the electron-transport chain.

72
Q

the name for a protein that can lyse red blood cells?

A

Hemolysin

73
Q

Which of the following features of Salmonella prevent it from being phagocytosed?

A

Flagella

74
Q

Where do Salmonella pathogens grow and replicate in the infected host?

A

Inside phagocytes

75
Q

How are immune cells able to detect foreign pathogens?

A

They are able to detect structures on the surfaces of foreign cells that are not found in the host.

76
Q

How does a capsule help certain bacteria evade detection by the immune system?

A

The capsule is composed of polysaccharides that are similar to those found in the host; thus, the immune system does not recognize it as foreign.

77
Q

TB bacterium grows where

A

Inside macrophage

78
Q

How does the protozoan Trypanosoma evade detection by the immune system?

A

It can change the surface antigens frequently, preventing the immune system from tracking it.

79
Q

An exotoxin that has the ability to kill or damage host cells is referred to as a(n)

A

Cytotoxin

80
Q

Which domain of the A-B toxin binds to cell surface receptors on the host cell?

A

B Domain

81
Q

How are superantigens different from other types of exotoxins?

A

Superantigens must be endocytosed into a target cell before becoming active.

82
Q

leukocidins

A

Molecules that are capable of destroying phagocytes

83
Q

How do superantigens enable pathogens to hide from the immune system if they actually stimulate the immune system?

A

They cause the immune system to produce an exaggerated response, distracting it from the actual pathogen.

84
Q

How can capsules enable bacteria to evade the immune system?

A

Capsules block the complement biding sites on the surface of the pathogen.

85
Q

Certain traits that allow pathogens to create infection and cause disease are termed

A

VIrulence factors

86
Q

Which of the following enzymes breaks down the “glue” that holds cells together?

A

Hyaluronidase

87
Q

How do fibrinolysins enhance a pathogen’s virulence?

A

They break down fibrin proteins that are involved in clot formation, allowing the cells to penetrate deep into damaged skin.

88
Q

Fever and NK cells are part of what line of defense

A

Second

89
Q

T and B lymphocytes are part of what line of defence?

A

Third

90
Q

Eosinophils phagocytic?

A

Yes, they are phagocytes

91
Q

Steps of phagocytosis

A

Chemostaxis
Adherence
Pseudopods engulf and internalize microbe forming phagosome
Lysosome and phagosome fuse and form phagolysosome
Digestion of microbe
Discharge of excess material

92
Q

How do microfilaments play a role in chemotaxis

A

Chemotaxis is brought about by the binding of various chemoattractant substances (microbial components, complement components, cytokines) to receptors on the surface of phagocytes. This triggers cell movement toward higher concentrations of the attractant. The interaction of actin microfilaments and myosin (cytoskeletal elements) within the phagocyte makes this movement possible.

93
Q

Strategies microbes use to avoid [hagocytosis

A

Produce leukocidin
Capsule
Preventfusion of phagosome with lysosome
Escape phagosome

94
Q

What does the plasma membrane of a phagocyte attach to on a microorganism?

A

Glycoproteins

95
Q

What is the role of opsonins?

A

They create “handles” that make it easier for the pseudopods of phagocytes to attach to the microbe invader.

96
Q

How is Streptococcus pneumoniae able to avoid destruction by a phagocyte?

A

Their capsules make them “slippery” to phagocytes.

97
Q

Which of the following microorganisms use M protein to avoid destruction of a phagocyte?

A

Streptococcus pyogenes

98
Q

If a new bacterial pathogen entered a human body through an accidental needle stick, the first cell that would try to kill the pathogen would likely be

A

a phagocyte.

99
Q

When does maturation occur in phagocytosis

A

After ingestion, before killing

100
Q

why the lectin or alternative pathway would stimulate a more immediate response than the classical pathway.

A

Neither pathway relies on antibodies.

101
Q

What direct effect do histamines and leukotrienes have on capillaries?

A

They allow capillary walls to open and become leaky.

102
Q

Cells from damaged tissues and the complement pathway both release

A

Histamenes

102
Q

Emigration is

A

the migration of phagocytes through blood vessels to the site of tissue damage.

103
Q

5 classes of antibodies

A

IgG
IgM
IgA
IgD*
IgE

104
Q

IgG

A

Produced as monomer
80% of all antibodies
Enhances phagocytosis (opsinization)
23 day life

105
Q

Most antibodies are

A

IgG

106
Q

IgM

A

Pentamer (5 antibodies held together into this large structure)
First antibodies produces in initial response to infection
Antigen binding sites are on outside, therefore this molecule can bind many antigens and can bring about agglutination of antigens (several antigens clumped together) and phagocytes easily able to grab onto these structures
5 day life

107
Q

IgA

A

Two antibodies joined together (dimer)
Found in secretions (mucous, saliva, milk, tears)
Provide localized protection in these specific areas
6 day life

108
Q

Which antibody is a pentamer

A

IgM

109
Q

IgE

A

Can bind to mast cells (histamine granules) causing release of histamines and basophils cells (responsible for meany allergic reactions)
Responsible for lysing large parasites (parastic worms)
2 day life

110
Q

How does pathogen recognition occur

A

When you encounter pathogen to thefirst time, pieces of the pathogen are take nto the lymphoma, and there they are tested against different T cells and B cells, and those that respond proliferate (clones) and each one that responds will now be ready if they encounter the pathogen again

They differentiate into long lived memory cells and short lived plasma cells

111
Q

Which antibody aids in opsinization

A

IgG

112
Q

Antibody titer

A

the amount of Ab in the serum
Two immonlogical responses

113
Q

When do IgM and IgG begin production after exposure to pathogen?

A

2-4 days

114
Q

When does IgM peak in primary encounter

A

10 days

115
Q

When does IgG peak in primary encounter

A

14 days

116
Q

What is the difference in curves in IgM and IgG

A

In primary encounter, IgM is produced quicker, but all is destroyed after encounter, and is replicated in second encounter

IgG Produced slower in intial encounter, but does not drop down to 0, therefore, secondary encounter the IgG antibodies remeber the antigen or a quicker stronger secondary response

117
Q

How many days untl IgG increases considerably in second encounter

A

5 days

118
Q

Do IgM and IgG recognize different antigens?

A

Both IgM and IgG recognize similar structures on antigens

119
Q

What would a third encounter immune response look like

A

Third time exposure results in a very similar response

120
Q

Agglutination

A

Antigen binds to multiples antibodies to cause it to be easier to spot by phagoccytes

Reduces number of antigens to be dealt with

121
Q

Opsinization

A

Complement proteins bind to pathogens helping phagocytes recognize antigens much better
Adherence of pathogen to phagocyte much greater (Handles)

122
Q

Neutralization

A

Bc toxins need to get INTO body to causes damage, but the presence of antibodies that bind to the toxins do not allow it to enter the cell
Bacteria and viruses normally need to interact with host cell to cause damage, coating them in antibodies prevent them from interacting with the cell

Blocks adhesion of bacteria and viruses to mucosa

123
Q

Activation of complement:

A

Two antibodies bind to pathogen. Complement protein binds to athe antibodies and becomes activiated, in doing this it attracts other complement proteins to the pathogen, and they start forming holes in the pathogen to cause lysis.

124
Q

Antibody-dependent cell-mediated cytotoxicity

A

Antibody that bind s to large parasite, attract WBCs, becomes activated to produces enzymes that damage the parstite membrane

125
Q

Two different chains on T cell receptors

A

Alpha and beta

126
Q

3 regions of an antibody

A

Constant, variable, and transmembrane regions

127
Q

What region of antibody provides specificty

A

Varibale region provide antigen specificity

128
Q

How does age affect a persons ability to make t cells?

A

Decrease with age

129
Q

Infected cell:

A

Factory for creating more viruses/pathogens

130
Q

Affected cell

A

Going crazy like cancer cells

131
Q

How do T cells act in an autoimmune disorder

A

When T cells cannot recognize affect/infected cells accurately, they can destroy healthy cells (auto immune disorder)

132
Q

MHC

A

Major histocompatibility complex (MHC) are genes that code for MHC proteins found on cell surface. Two major classes of MHC proteins

133
Q

Class 1 MHC

A

Found on all nucleated cells in the body (of infected cells - declare that they are infected
Identify self
They display peptide antigens TO cytotoxic T-cells - these T cells destory the infected cell

134
Q

Class II MHC

A

Proteins located on Antigen presenting cells

Dendtric cells, macrophages, and B-cells

Display antigens to Helper T cells and Cytotoxic T cells

135
Q

APCs

A

Digest and process cells and then display a mark on the surface of them so that other cells can recognize them

136
Q

How are T cells distinguished

A

Distutished by proteins on cell surface called “clusters of differentionaton (CD) antigens

137
Q

Helper T-cell

A

CD4 Cells
65% of mature lymphocytes
Bind to MHC class II on APCs to activate B and T cells
HIV attacks/destroy CD4 cells

138
Q

Cytotoxic T-cells

A

CD8 Cells
35% of mature T lymphocytes
Binds to MHC class 1 on infected self cells (being displayed by MHC class 1 proteins on the surface of infected cell) to activate cell apoptosis (programmed cell death)

139
Q

How do MHC 1 cells behave when infected

A

they take bits and pieces of antigen and display them on there MHC class 1 proteins

140
Q

What is the double recognition of T cells

A

Bind to antigen receptor and reconize how the cell should look

Recognize MHC 1 or 2

141
Q

What occurs if infected cell displays antigen of MHC 1 protein

A

If there is an antigen being displayed, the antigen receptor will see it and generate the reaction (cell aptosisis)

Cytoxic T cells go around checking cells, regardless if they are infected or not

142
Q

What do Helper T cells do

A

After Dendritic Cell engulfs pathogen it displays antigen fragments on MHC class 2 on their surface

Helper T binds with MHC, the recognition of antigen fragments causes secretion of cytokines by APC cell

Helper T cell proliferates, all with receptors for MHC antigen fragment complex

H T cells secrete cytokines activating B cells and cytotoxic T cells

B cells differentiate to remember antigen for future and C T cells destroy infected cell

143
Q

How does a helper T cell act on a B cell

A

B cell internalizes antien, displays antigen fragment on MHC 2

Helper T cell with specific receptors for fragement binds and activates B cell

B cell proliferates and differentiates into memory B cells and antibody secreting plasma cells

Antibodies produced are specific to for the antigen that started the response

Without helper T cell, B-cell would do this process on it’s own, but helper T cell comes in to help it to the job better

144
Q

How are affected cells dealt with

A

Cytotoxic T cells would recognize them by abnormal structures (antigens) being displayed on the MHC class 1, therefore these cells are also destroyed
Cells that are going crazy all the time, but we don’t notice

145
Q

Why are transplants problematic

A

All cells in the body with a nucleus have MHC class 1 proteins
These are the proteins the distinguish all your cells from someone elses
This is the problem with transplants
Immunosuppressants act to try and reduce the recognition of new cells by Cytotoxic T cells (double recognition)

146
Q

How do C T cells kill

A

Recognize infected cells and secrete proteins (perforins) that form holes in infected cells- destroying infected cells

147
Q
A

BIO233 (18 decks)

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