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Immunology Flashcards

1
Q

Immune System

A

Collection of cells, tissues, and molecules that mediate resistance to foreign elements (antigens)

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2
Q

Immune response

A

Coordinated reaction of these cells and molecules to antigens

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3
Q

Immunology

A

Study of the immune system, including its responses to microbial pathogens and damaged tissues and its role in disease

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4
Q

Antigen

A

Antibody generator

Molecules that induce an immune response when introduced into the body

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5
Q

Epitope or antigenic determinant

A

Part of an antigen that is actually responsible for inducing the immune response and binding to the products of the immune response (lymphocyte receptors and antibodies)

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6
Q

Self versus non-self

A

The immune system must be able to discriminate foreign elements from components of its own organism
Failure results in autoimmunity
Immune responses should be generated only when components of the immune system come into contact with non-self elements

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7
Q

Innate Immunity

A

Physical barriers
Inflammation
Complement

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8
Q

Adaptive immunity

A

Humoral immunity

cellular immunity

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9
Q

Innate Immunity: Activation

A

Always active

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10
Q

Innate Immunity: main cells

A

Macrophages, neurophils, NK cells

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11
Q

Innate Immunity: Response time

A

Fast (minutes to hours)

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12
Q

Innate Immunity: specificity

A

Structures common to several pathogens

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13
Q

Innate Immunity: Memory

A

Absent

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14
Q

Adaptive immunity: Activation

A

Only when in contact with antigens

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15
Q

Adaptive immunity: main cells

A

T cells and B cells

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16
Q

Adaptive immunity: Response time

A

Slow (days to weeks)

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17
Q

Adaptive immunity: Specificity

A

Specific antigens

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18
Q

Adaptive immunity: Memory

A

Present

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19
Q

Physical/ Chemical Barriers

A

things like pH of intestinal tract, mucus in respiratory system
Antimicrobial properties-prevent infection from taking place

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20
Q

Recognition of Pathogens

A

Pathogen-Associated molecular patterns (PAMPs)
Components that are shared between different types of pathogens and present a molecular composition that differ from self

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21
Q

Recognition of Damage

A

Damage-associated molecular patterns (DAMPs)
Released when cells die (intracellular DAMPs) or generated when connective tissue is damaged (extracellular DAMPs)

No DAMPs if cells die of apoptosis

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22
Q

Pattern Recognition Receptors

A

Receptors of innate immunity that recognize PAMPs and DAMPs
Soluble or membrane-bound
signaling phagocytic

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23
Q

Cells of the immune system

A

Many share some precursor cells
all start from a stem cell
Some cells will have multiple functions

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24
Q

Neutrophils: Appearance

A

Segmented nucleus, granular cytoplasm

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25
Q

Neutrophils: Location in health

A

Blood

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26
Q

Neutrophils: Lifespan

A

48-72 hours

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27
Q

Neutrophils: Primary Function

A

Antimicrobial effectors, particular in acute bacterial infection (innate)

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28
Q

Neutrophils: Mechanism of Action

A

Phagocytosis; degranulation; Neutrophil extracellular trap formation

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29
Q

Eosinophils: Appearance

A

Characteristic eosinophilic granules

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30
Q

Eosinophils: Location in health

A

Blood and tissues lining gastrointestinal tract and airways

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31
Q

Eosinophils: Lifespan

A

Days to weeks

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32
Q

Eosinophils: Primary Function

A

Antiparasitic effectors, particularly in helminthic infection; some antiviral action; roles in allergy (innate)

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33
Q

Eosinophils: Mechanism of Action

A

Degranulation; Limited phagocytosis

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34
Q

Basophils: Appearance

A

Characteristic blue-purple basophilic granules

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35
Q

Basophils: Location

A

Blood

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36
Q

Basophils: Lifespan

A

Days

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37
Q

Basophils: Primary function

A

Mediatory of inflammation (innate)

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38
Q

Basophils: Mechanism of action

A

Degranulation

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39
Q

Mast Cells: Appearance

A

Round nucleus, cytoplasm densely packed with purple granules

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40
Q

Mast Cells: Location

A

Tissue, particularly connective tissue surrounding vasculature and nerves, and the lamina propria of the mucosa

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41
Q

Mast Cells: Lifespan

A

Weeks to months

42
Q

Mast Cells: Primary function

A

immune surveillance, mediator and amplifier of inflammation and allergy (innate)

43
Q

Mast Cells: Mechanism of action

A

Detection of threats and release of inflammatory mediators via degranulation (vasoactive amines) or synthesis of lipid mediators and cytokines

44
Q

Macrophages: Appearance

A

Round nucleus, clear-vacuolated cytoplasm, irregular cell shape

45
Q

Macrophages: Location

A

Peripheral Tissue

46
Q

Macrophages: Lifespan

A

Months

47
Q

Macrophages: Primary function

A

immune surveillance, moderate antimicrobial capacity, limited antigen presentaion

48
Q

Macrophages: Mechanism of action

A

Detection of threats and release of inflammatory mediators; phagocytosis

49
Q

Dendritic Cells: Appearance

A

Round Nucleus, clear cytoplasm, irregular shape with long branched projections (dendrites)

50
Q

Dendritic Cells: Location

A

Tissues

51
Q

Dendritic Cells: Lifespan

A

Months

52
Q

Dendritic Cells: Primary Function

A

Immune surveillance, antigen processing and presentation (adaptive)

53
Q

Dendritic Cells: Mechanism of action

A

Detection of threats and release of inflammatory mediators; endocytosis and phagocytosis

54
Q

Natural Killer (NK) cells: Appearance

A

Large lymphoid cell, round nucleus, azurophilic cytoplasmic granules

55
Q

Natural Killer (NK) cells: Location

A

Blood, spleen

56
Q

Natural Killer (NK) cells: Lifespan

A

Months

57
Q

Natural Killer (NK) cells: Primary function

A

Destruction of virally infected or abnormal host cells (including tumor cells) (innate)

58
Q

Natural Killer (NK) cells: Mechanism of action

A

Recognition of virally infected or abnormal host cells and targeted release of cytotoxic granules

59
Q

Lymphocytes: Appearance

A

Round nucleus, clear cytoplasm, high N:C ratio

60
Q

Lymphocytes: Location

A

Blood, tissues, secondary lymphoid organs

61
Q

Lymphocytes: Lifespan

A

Weeks to months, years (memory cells)

62
Q

Lymphocytes: Types

A 
T cells (TCR)
B cells (BCR)
Both will have a specific receptor characteristic of that lymphocyte
Their specific epitope
63
Q

Complement System

A

Collection of plasma proteins that are individually inert but can interact in a cascade once they are activated
Attacks the cellular membrane leading to cell death
Act as signaling molecules that recruit immune cells to inflammatory sites

64
Q

Cell communication: Receptors

A

Expressed in the surface of a cell or in intracellular compartments

65
Q

Cell Communication: Ligands

A

Molecules that activate receptors

Soluble or membrane-bound

66
Q

Cell Communication: Cytokines

A

Proteins with diverse functions such as cell growth, activation
Interleukins- communication between cells
Chemokines- chemotaxis
(kinda start with cell that hasnt figured out its life- depending on whats going on, and what cytokines are present will affect what the cell becomes

67
Q

Inflammation: recognition of threat

A

Pathogen-Associated Molecular Patterns
Damage-associated Molecular Patterns
The first thing that needs to happen. These are what the cells need to recognize

68
Q

Sentinel cells

A

Dendritic cells, Macrophages, Mast cells -> pro-inflammatory and antimicrobial mediators
Sentinel cell exposed to PAMPs, DAMPs, or pro-inflammatory cytokines

detect PAMPs, DAMPs, and release mediators that will activate an inflammatory response- effect macrophages, plasma proteins -> affects complement system

69
Q

Sentinel Cell Activation

A

Upregulation of cellular antimicrobial defenses

Release of proinflammatory chemokines, lipid mediators, and cytokines

70
Q

Inflammation: Mast cells

A

Vasoactive molecules (histamine, serotonine)
Vasodilation
Increased vascular permeability
All these mediators and leukocytes to get to injury site (usually in tissue) done so by blood
More leukocytes arriving
Increase blood flow (Swelling)- slower velocity
Easier to migrate to tissue

71
Q

Systemic consequences: Hypothalamus

A

Fever, anorexia, sleepiness, depression

72
Q

Systemic consequences: Liver

A

Increases synthesis of acute-phase proteins

Iron sequestration

73
Q

Systemic consequences: Bone

A

Increases white cell production

74
Q

Leukocyte extravasation

A

Macrophages and dendritic cells, produce cytokines such as that activate the endothelial cells to express selectins and ligands for integrins and to secrete chemokines
Selectins -> rolling
Integrins -> adhesion
Chemokines -> migration

Macrophages in tissue, stimulated by microbes and will produce mediators (cytokines etc) and will have an effect on vessel walls
Mast celss stimulating dilation which helps leukocytes arrive
some cytokines will cause some endothelial cells to express certain molecules (selectins and integrins)

75
Q

Leukocyte Chemotaxis

A

Neutrophils will extend pseudopods to fell around for inflammation site

76
Q

Leukocyte kinetics during inflammation

A

Lymphocytes are present once the adaptive immune system is engaged in the response
Monocytes/Macrophages predominate at later stages of inflammation
Neutrophils predominate during acute inflammation

77
Q

Phagocytosis

A

It is an active process of capturing and ingesting foreign objects/microorganisms by phagocytes- neutrophils and macrophages
Destruction of microorganisms, damaged cells and cellular debris, foreign objects
Induction of cytokine production
Processing and presentation of antigens (macrophages)

Recognition of microbe
Endocytosis
Phagosome maturation
Fusion of phagosome and lysosome
Killing of bacteria inside the phagolysosome
78
Q

Intracellular Killing Mechanism: Oxidative Pathway

A

Use fo oxygen and glucose increases several fold “respiratory burst”
Reactive oxygen species (ROS)
Reactive nitrogen species (RNS)
Toxic to microorganisms

79
Q

Intracellular Killing Mechanism: Non-oxidative

A

Dependent on the action of the toxic substances present in lysosomes
Cationic proteins: damage the bacterial cell wall
Lysozyme: damages the mucopeptides in the bacterial cell wall
Lectoferrin: Sequestrates iron thus inhibiting bacterial growth
Preoteolytic and hydrolytic enzymes: digest killed bacteria

80
Q

Extracellular Killing by NETs

A

Neutrophil Extracellular Traps
Increase in proinflammatory stimulus
Extrude strands of nuclear DNA and associated proteins into the extracellular fluid
Traps and kills microbes

81
Q

Complement System

A

Collection of circulating and membrane-associated proteins
Many complement proteins are proteolytic enzymes
Activation occurs in a sequential manner

3 pathways:
Alternative pathway
Classical Pathway
Lectin Pathway

82
Q

Alternative Pathway

A

Complement proteins are activation on microbial surfaces (because complement regulatory proteins are not present on microbes, only on host cells)
Activated by innate

83
Q

Lectin Pathway

A

Activated when a carbohydrate-binding plasma protein, mannose-binding lectin (MBL), binds to terminal mannose residues on the surface of glycoproteins
Innate

84
Q

Classical Pathway

A

Activated by antibodies that bind to microbes or other antigens
First described, last to kick in
Adaptive immune system

85
Q

Membrane attack complex

A

How does the complemet system kill cells
Breached the cell membrane of the microbe, allowing water to rush in by essentially punching holes which creates cylindrical pores
Destruction bt osmotic lysis

86
Q

Type 1 Interferons

A

Innate immunity
One of the cytokines
Produced by virus-infected cells and plasmocytoid DCs
Non-specific response to viral infections
IFN-a and IFN-B: inhibit viral replication and induce antiviral state
effects the cells metabolism so it cant synthesize proteins correctly

87
Q

Natural Killer Cells

A

Recognize and respond to infected and stressed cells
A. killing of the cells
B. Secretion of IFN-y stimulates and activates macrophages.
First line of defense against tumors.

Healthy host cells express self class I major histocompatibility complex (MHC) molecules, which are recognized by inhibitory receptors

NK cells are activated by infected or mutated cells in which ligands for activating receptors are expressed (often at high levels) and class I MHC expression is reduced
NK cells are checking to make sure the cells have MHC I
88
Q

Adaptive Immunity

A

T and B cells
Will have specific antigen receptors (epitopes)
Driving a much more specific response

89
Q

Antigen processing and Presentation

A 
Major histocompatibility complex (MHC) molecules
2 types: class 1 MHC
class 2 MHC
These are similar with slight differences. Both are there to help present an antigen to a T cell. Differences are in types of cells that contain them and to which type of T cell theyll present the antigen
T calls can only recognize antigens presented in an MHC molecule- cant do it on their own
90
Q

Class I MHC

A 
All nucleated cells have MHC I- response to intracellular pathogens- important to be able to eliminate pathogen no matter what cell its in
Cytosolic protein- antigen uptake by proteasomes and processed and broken down to peptides. These peptides will bind to class I MHCmolecules on ER. Transported to cell membrane and MHC can present the peptide to T-cells
MHC I presents antigens ONLY to CD8 T cells (cytotoxic T lymphocytes)
91
Q

Class II MHC

A

Break down proteins-pick them up through endocytosis. Use lysosomes to break down then bind to MHC II and transported to membrane and presented to T cells (T helper) doesnt kill it but will stimulate other cells that will ]MHC II presents antigens to CD4 T cells (T helper cells
MHC II expressing cells are professional antigen presenting cells (APCs): dendritic cells, macrophages, B cells

92
Q

Activation of Naive T cells

A

Always done by a dendritic cell
Dendritic cell will prime and activate naive T cells. Dendritic cell can do MHC I and II so it can activate CD8 (no response after- the cell will just be killed) and CD4 activation
Then they will have proliferation- specific T cell clone
Then Differentiation- effector and memory T cells.

Immature DCs encounter antigens in tissues
Migration to lymphoid tissue and maturation
Antigen presentation by mature DCs in lymph nodes

93
Q

Differentiation of activated T Cells

A

Subsets: CD4+

CD8+

94
Q

CD4+

A

Th1, Th2, Th17

Express surface molecules and secrete cytokines that activates other cells

95
Q

CD8+

A

Cytotoxic T lymphocytes (CTLs_
Killing of infected cells
endpoint

96
Q

Cellular response: CD4+ Th1 cells

A

cytokine secretion
causes activation of macrophages and phagocytosis to kill microorganisms
activation of CTLs (CD8+)

97
Q

Cellular response: CD8+ CTLs

A

Induces apoptosis of infected cells

98
Q

Humoral response: B cells

A

Basically the antibody response

Able to recognize antigens independently of MHC presentation
Activated by Th cells or T-independent activation (need Th in order to amount FULL immune response)
B cells only produce IgM, but with Th can do isotype– switch to do other.
Differentiate between effector (plasma) cells and memory cells( not in T-independent) (plasma might change type of antibody they secrete)
Affinity maturation (not in T-independent) over course of immune response, the antibodies being produced by those cells will become of higher affinity by the epitope than they were in initial stages

99
Q

Humoral Response: Immunoglobulins

A

Isotypes or classes:
IgM (blood), IgG (blood and tissues), IgA (mucous membranes), IgE (epithelial tissue), IgD
Only B cells will produce antibodies so Ig are the B cell receptors themselves

100
Q

Isotype Comparasin

A

Differences in heavy chain structure, monomeric vs polymeric, subclasses, serum concentration, half-life, functions

101
Q

Humoral response against microorganisms

A

B cells will have receptors on membrane and get activated and can produce receptors in soluble form.

Against microorganisms or toxins:
bind them and neutralize them
Facilitate action phagocytic cells- can cover microbes
Trigger NK cell activation
Antibody dependent cellular cytotoxicity
102
Q

Primary and Secondary Ab response

A

IgM is the major Ab of primary responses. Acute infection. first one to increase because all cells can make IgM
IgG is the major Ab of secondary responses. Chronic infection

PID (14 decks)

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