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MICR 270 > Module 2 > Flashcards

Module 2 Flashcards

1
Q

innate immunity

A
  1. first line of defense against foreign invaders
  2. operated non-specifically during early phases of an immune response, without the need for prior exposure to the invading pathogen
  3. fights all pathogens in the same way and is ready to be mobilized upon the first signs of infection
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2
Q

sub-sections of the innate IS

A
  1. immune barriers
  2. inflammation
  3. pattern-recognition
  4. phagocytosis
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3
Q

immune barriers sub-section of innate IS

A

immune system is made of physical, soluble and cellular barriers that are scattered throughout the body

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4
Q

inflammation - sub-section of innate IS

A

innate immunity responds immediately to an invading pathogen

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5
Q

inflammatory response

A

the first immune response events following the breach of the physical barrier by a pathogen

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6
Q

pattern-recognition sub-section of innate IS

A
  1. innate IS recognizes general patters not specific for any one antigen
  2. this is largely performed by pattern-recognition receptors (PRR) exposed on innate immune cells
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7
Q

phagocytosis sub-section of innate IS

A
  1. some immune cells have phagocytic properties
  2. the group of cells sharing those abilities are called phagocytes
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8
Q

3 types of immune barriers

A
  1. physical
  2. cellular
  3. soluble
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9
Q

physical immune barrier

A
  1. made of every structure located at the interface between the inside and outside of the body (prison walls)
  2. made of physical and chemical components
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10
Q

examples of physical immune barrier

A
  1. skin
  2. cilia
  3. bodily secretions
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11
Q

primary function of the physical immune barrier

A

prevent or slow down the invasion of pathogens

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12
Q

physical components to the physical immune barrier

A
  1. the skin is the largest organ of the body and it creates a barrier that pathogens cannot cross unless it is breached
  2. mucous membranes cover the cavities of the body including the respiratory, gastrointestinal, urinary, and reproductive tracts
  3. these membranes contain specialized stuctures such as cilia and produce mucous
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13
Q

cilia

A

hairlike vibrating structures that can trap particles, preventing them from reaching vulnerable areas of the mucous membrane

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14
Q

mucous

A

viscous substance secreted by mucous membranes

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15
Q

mucous and cilia working together as physical immune barrier

A
  1. microorganisms get caught in sticky mucous which prevent them from reaching the lungs
  2. then the cilia of the respiratory tract sweep these organisms up and out of the body through coughing or sneezing
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16
Q

chemical components to the physical immune barrier

A
  1. tears and saliva are mucous membrane secretions which contain active antimicrobial substances such as lysozyme
  2. gastric acid destroys most bacteria and toxins that enter the stomach
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17
Q

lysozyme

A

an enzyme that catalyzes the destruction of the cell walls of certain bacteria

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18
Q

gastric acid

A

digestive fluid formed in the stomach (pH ~2.5)

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19
Q

cellular immune barrier

A

made of the various cells that play a role in the innate immune response
(prison guards)

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20
Q

examples of the cellular immune barrier

A
  1. neutrophils
  2. macrophages
  3. dendritic cells
  4. natural killer cells
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21
Q

primary function of the cellular immune barrier

A

prevent or slow down the invasion of pathogens that have broken through the PHYSICAL BARRIER

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22
Q

neutrophils

A

most common leukocyte found in blood of mammals (~45-70%)

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23
Q

function of neutrophils

A
  1. phagocytes that patrol the body to find, engulf and destroy pathogens
  2. circulate in the blood for ~12hrs before entering tissues by diapedesis
  3. recruited to a site of infection by resident macrophages that have encountered pathogens
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24
Q

lifespan of neutrophils

A

1-3 days after entering the tissues

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25
Q

macrophages

A
  1. phagocytes that patrol the body to find, engulf and destroy pathogens
  2. can either take up residence in a specific tissue, or move freely/patrol throughout a larger area of tissues
  3. contribute to tissue repair and present antigens to other immune cells such as T-cells
  4. become activated after phagocytosing pathogens or in response to cytokine signaling
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26
Q

dendritic cells

A

phagocytes that are often in contact with the external environment (specifically Langerhans DC)

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27
Q

function of dendritic cells

A
  1. engulf foreign antigens that have invaded the initial barriers of the innate immune system
  2. present antigens on their cell surface through peptide: MHC complexes, which can be recognized by helper T-cells
  3. major link between innate and adaptive immune systems
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28
Q

functions of natural killer cells

A
  1. recognize abnormal cells lacking antigen-specific receptors
  2. destroy abnormal cells of the body, which include tumorous and virus-infected cells
  3. bind to cell surface of target cells and release chemicals causing pores to form in the cell membrane, leading to lysis
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29
Q

soluble immune barrier

A
  1. made of macromolecules which contribute to the mediation of an innate immune response (communication system)
  2. play a key role in the development of an inflammatory innate immune response, which is induced following the penetration of an infectious agent through the bodys physical barriers
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30
Q

examples of soluble immune barrier

A

complement and cytokines (two categories of the macromolecules)

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31
Q

complement system

A

made up of over 30 soluble proteins

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32
Q

functions of the complement system

A
  1. complement proteins circulate in the blood normally in an inactive form
  2. can be directly activated in the presence of extracellular pathogens or indirectly by pathogen-bound antibody
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33
Q

what does activation of the complement system induce?

A

induce a cascade of reactions between various complement proteins, leading to formation of MAC and in parallel enhances, or complements the efficiency of other immune functions, such as inflammation and phagocytosis

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34
Q

3 major pathways the complement system can be activated

A
  1. classical
  2. alternative
  3. lectin
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35
Q

inflammation process of the complement system

A
  1. includes attraction of various immune cells in the site of infection through release of chemotactic molecules (histamine and cytokines)
  2. activated CP bing to complement receptors on immune cells, such as mast cells and basophils, inducing the release of these substances which enhance the inflammatory response
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36
Q

chemotactic molecules

A

inducing the movement of cells toward the site where the substances are originally released

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37
Q

phagocytosis of the complement system

A

activated complement proteins mostly C3b, opsonize pathogens thereby targeting them for destruction by phagocytosis

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38
Q

opsonize

A

making a foreign particle more susceptible to phagocytosis by binding to the antigen and marking for ingestion

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39
Q

membrane attack complex (MAC) of complement system

A
  1. destroy extracellular foreign invaders through the formation of membrane attack complexes
  2. create holes in the pathogen which leads to its lysis and death
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40
Q

main functions of the complement system

A
  1. opsonization which induces phagocytosis
  2. chemotaxis which induces inflammation
  3. lysis through its MAC
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41
Q

cytokines

A
  1. small proteins secreted by various immune cells in response to a number of different stimuli
  2. chemical mediators that play a key role in cell-to-cell communication
  3. strong affinity for specific type of cytokine receptor
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42
Q

what is the function of cytokine signalling?

A

regulate immune processes, such as immune responses, inflammation and hematopoiesis

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43
Q

characteristics if cytokines

A
  1. autocrine vs. paracrine vs. endocrine
  2. specificity and affinity
  3. alter gene expression
  4. pro-inflammatory vs. anti-inflammatory
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44
Q

autocrine

A

sending and receiving cell is the same

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45
Q

paracrine

A

sending and receiving cells are near each other

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46
Q

endocrine

A

sending and receiving cells are distant from each other

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47
Q

where do the majority of cytokines act?

A

locally, having an autocrine or paracrine effect

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48
Q

what do auto, para and endocrine characterize?

A

the location of action depending on the site of secretion of cytokines by an immune cell

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49
Q

specificity and affinity of cytokines

A
  1. cytokines bind to specific receptors on the membrane of their target cells
  2. cytokines and their receptors exhibit very high affinity for one another
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50
Q

ligand

A

biological molecule that attaches to a protein (receptor) to induce a signal

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51
Q

alter gene expression (cytokines role)

A

binding of cytokine to its receptor initiates a series of reactions that ultimately alter gene expression
- this may affect cell growth and maturation and have lots of roles in the hosts response to infection and disease

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52
Q

pro-inflammatory cytokines

A
  1. made by most immune cells
  2. when secreted these cytokines will induce an inflammatory response within the body
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53
Q

anti-inflammatory cytokines

A
  1. made by several immune cells
  2. work to limit the inflammatory response within the body by inhibiting pro-inflammatory cytokine production and activating the immune cells that promote healing
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54
Q

what happens if pro-inflammatory cytokines are not properly controlled?

A

leads to complication such as tissue damage due to an excessive inflammatory state

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55
Q

what happens if anti-inflammatory cytokines are not properly controlled?

A

a lack of an immune response to pathogen may occur which can result in spreading of the pathogen

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56
Q

inflammation

A
  1. occurs in response to a pathogen invading the physical barrier of the innate immune system
  2. series of biological reactions to invasion of harmful infectious agents into the body
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57
Q

characterization of inflammation

A
  1. redness
  2. pain
  3. heat
  4. swelling
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58
Q

steps of inflammation

A
  1. Alteration of blood flow to the injured area
  2. Influx of phagocytic and other immune cells
  3. Removal of foreign antigens
  4. Healing of damaged tissue
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59
Q

physical response of inflammation

A

can result in a loss of function

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60
Q

purpose of inflammation

A
  1. body’s attempt at self-protection by removing harmful stimuli, including damaged cells, irritants, or pathogens
  2. purpose is to localize and eliminate the invading pathogen, in an effort to stop it from spreading, and to remove damaged tissue
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61
Q

major events of inflammation process

A
  1. breach
  2. vasodilation
  3. permeabilization
  4. extravasation
  5. phagocytosis
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62
Q

breach - inflammation

A
  1. pathogens must find a breach in order to be able to enter the body due to the physical barrier being sealed
  2. can occur via a wound created by a nail or glass
  3. will damage cells and give opportunity for pathogens
    to break through the physical barrier
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63
Q

vasodilation - inflammation

A
  1. first major event
  2. increase in diameter of the blood vessels, and permeabilization
    of the capillaries near the affected area
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64
Q

what does vasodilation in inflammation induce?

A

physiological changes by vasoactive and chemotactic factors secreted by damaged tissues and activated immune cells, such as macrophages and mast cells

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65
Q

typical consequences of vasodilation in inflammation?

A

redness and heat
- induces a higher blood volume around the infected tissue

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66
Q

vasoactive

A

components affecting the diameter
of blood vessels

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67
Q

chemotactic factors

A

components inducing the movement of cells in response to a chemical stimulus

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68
Q

permeabilization - inflammation

A
  1. allows accumulation of excess fluid at the site of infection called exudate
  2. includes both pro-inflammatory cytokines (specifically chemokines) and complement proteins that will be activated in the presence of the extracellular pathogens
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69
Q

exudate fluid

A

contains proteins that contribute to the mediation of inflammatory response

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70
Q

what is the function of the proteins in permeabilization?

A

to attract the cellular barrier key players to site of infection

71
Q

swelling in permeabilization

A

is a consequence of accumulation of fluids at infection site, forming what is called an edema

72
Q

extravasation - inflammation

A
  1. the chemotactic factors released by cells during vasodilation and permeabilization steps induce the recruitment of more immune cells to site of infection
73
Q

what are the first type of cells to arrive by chemotaxis to site of infection?

A

neutrophils

74
Q

neutrophils arriving to infection site - extravasation

A

when neutrophils that are circulating in the blood arrive to an infection site,
they adhere to the endothelial cell walls via MARGINATION and
migrate between the capillary-endothelial cells into the infected tissue by EXTRAVASATION or DIAPEDESIS

75
Q

phagocytosis - inflammation

A
  1. at infection site, neutrophils and other phagocytes (macrophages and dendritic
    cells) engulf the pathogens
  2. destroys extracellular pathogens
  3. in innate IR is not effective in neutralizing the threat, the adaptive IR will be induced
76
Q

correct order in which the inflammatory response steps occur

A
  1. vasodilatation
  2. permeabilization
  3. chemotaxis
  4. margination
  5. extravasation
77
Q

the inflammatory response (3 D’s)

A
  1. detect
  2. deflect
  3. destroy
78
Q

symptoms if illness with inflammation

A

signs of healing

79
Q

pus

A

made of neutrophils - most common phagocyte

80
Q

what happens to neutrophils after destroying a pathogen?

A

they self-destroy

81
Q

how do macrophages destroy pathogens?

A

macrophages use cytoplasmic extensions to destroy pathogens and can do this repeatedly

82
Q

how do natural killer cells destroy pathogens?

A

protrude them

83
Q

fever

A

macrophages come after neutrophils to take over, if they don’t work they release pyrogen chemicals that tap the hypothalamus and raise your body temperature to burn everything
- adaptive immune defences come in after

84
Q

how does heat induce healing?

A

increases the metabolic rates of cells allowing them to repair themselves faster

85
Q

how does swelling induce healing?

A

swelling leaks proteins, which help clot blood and form scabs
- also recruits local phagocytes and lymphocytes to help destroy pathogens and clean up dead cells

86
Q

pattern recognition receptors (PRRs)

A
  1. capable of recognizing repeated molecular patterns of pathogens
  2. can be expressed by both innate and adaptive immune cells (mostly innate)
87
Q

families of PRRs

A
  1. C-type lectin receptors
  2. NOD-like receptors
  3. toll-like receptors (TLRs)
88
Q

molecular pattern

A
  1. recognized by PRRs
  2. conserved motifs and certain subsets that can be found in various groups of pathogens, where they are called Pathogen-Associated Molecular Patterns (PAMP’s)
89
Q

pathogen-associated molecular patterns (PAMPs)

A

molecular structures either expressed on the surface of or found inside pathogens

90
Q

examples of PAMPs

A
  1. lipopolysaccharides (LPS) are found on cell surface of gram-negative bacteria
  2. double-stranded RNA found inside dsRNA viruses
91
Q

2 major categories of molecular patterns recognized by PRRs

A
  1. pathogen-associated molecular patterns (PAMPs)
  2. danger-associated molecular patterns (DAMPs)
    ***play a key role in ability of innate immune cells to recognize invaders
92
Q

PAMPs

A

molecules associated with groups of pathogens that are recognized by immune cells

93
Q

what do PAMPs include

A
  1. functional structures of pathogens
  2. repeated sequences of protein, glycoprotein, lipoprotein, amino acids, etc that are conserved across specific groups of microbes
    ***allows to initiate a quick response to infection by inducing an innate IR
94
Q

DAMPS

A
  1. molecules released by stressed cells undergoing necrosis
  2. are host biomolecules
  3. indicate damage to the body
  4. initiate an inflammatory response
95
Q

examples of DAMPs

A
  1. abnormal location of a cell structure (DNA found outside of mitochondria of nucleus)
  2. cell-stress indicator molecules (heat-shock proteins)
96
Q

necrosis

A

morphologic changes that accompany death of cells and that release large amounts of intracellular components to the environment

97
Q

toll-like receptors (TLRs)

A

class of PRRs whose signaling plays an essential role in the innate IR

98
Q

where are TLRs expressed?

A
  1. plasma membrane
  2. endosomal/lysosomal membranes of mammalian cells
    (depends on type of PAMP or DAMP)
99
Q

what do TLRs initiate the transcription of genes?

A
  1. inflammatory cytokines
  2. chemokines
  3. costimulatory molecules
    *** these contribute to the activation of innate immune cells, which increase the ability of phagocytes to engulf pathogens and enhance their ability to present antigens to adaptive IS
100
Q

2 major roles of TLRs

A
  1. recognize PAMPs and/or DAMPs
  2. induce expression of signalling to activate T-cells
101
Q

how do TLRs sense the presence of an infection?

A

through recognition of PAMPs and/or DAMPs

102
Q

TLR signalling process

A
  1. after engulfing bacterium, immune cell (APC) will present pieces of the pathogen (antigens) on its cell surface
    through the peptide: MHC complex
  2. APC will increase its production of
    costimulatory molecules, which are involved in the strength
    and stability of the antigen presenting process
  3. an immunocompetent naïve T cell specific for the antigen presented by the dendritic cell will bind to the peptide: MHC complex through its TCR
    - this interaction will activate and initiate an adaptive IR
103
Q

phagocytosis

A

second line of defence against the invading pathogen within innate immunity
- type of endocytosis, in which a cell takes up particulate material (such as bacteria) from its environment by invaginating its membrane to form a vacuole

104
Q

what are the ways phagocytosis can be induced?

A
  1. the recognition of a PAMP by a phagocyte through its PRR
  2. through pathogen opsonization
105
Q

major innate immune cells involved in maintaining cellular barrier

A
  1. neutrophils
  2. macrophages
  3. DCs
106
Q

neutrophils

A
  1. first cells to arrive from blood to site of infection
  2. perform early phagocytosis, eliminating pathogen quickly
  3. can initiate an inflammatory response
107
Q

macrophages

A
  1. migrate from the blood to tissues to become macrophages
  2. perform phagocytosis most efficiently (called “big eaters”)
  3. release cytokines that stimulate inflammation and recruit other immune cells
108
Q

dendritic cells

A
  1. recognize microbes and initiate phagocytosis
  2. most efficient antigen presenting cell
  3. play a major role in the initiation of the adaptive immune response
109
Q

steps of phagocytosis

A
  1. attachment
  2. ingestion
  3. fusion
  4. digestion
  5. release
110
Q

attachment - phagocytosis

A

pathogen becomes attached to membrane
evaginations called pseudopodia

111
Q

ingestion - phagocytosis

A

pathogen is ingested, forming a vacuole,
called phagosome within the cell

112
Q

fusion - phagocytosis

A

phagosome fuses with a lysosome, releasing
lysosomal enzymes that degrade macromolecules
and other materials, such as bacteria

113
Q

digestion - phagocytosis

A

pathogen is destroyed and digested by the lysosomal enzymes

114
Q

release - phagocytosis

A

digestion products are released from the cell via exocytosis

115
Q

exocytosis

A

process in which the vacuole membrane fuses with
the cell membrane

116
Q

evaginations

A

a protruding structure produced by turning a membrane outward

117
Q

adaptive IS

A
  1. second line of defence against foreign invaders
  2. longer time to initiate
  3. creates specific response against pathogens
  4. produces memory cells that will be able to respond faster and stronger in case if re-infection
118
Q

main characteristics of the adaptive IS

A

specificity and diversity

119
Q

specificity

A
  1. cells recognize one specific epitope of a pathogen
  2. creates a unique immune reaction to eliminate the infectious agent
120
Q

diversity

A

adaptive IS is composed of countless numbers of cells to be able to fight any pathogen encountered

121
Q

humoral immunity

A

B-cells and antibodies

122
Q

cell-mediated immunity

A

T-cells

123
Q

B-cell

A
  1. key component of humoral response
  2. mature in the bone marrow
  3. get so tired they want to die off but Helper T-cells tell them to keep going
124
Q

surface receptor of B-cells

A

B-cell receptor (BCR)

125
Q

function of B-cells

A

antibody factory

126
Q

subsets of B-cells

A
  1. plasmocyte
  2. mamory B-cell
127
Q

plasmocyte

A
  1. effector cell
  2. produce large quantities of antibodies
128
Q

memory B-cell

A
  1. memory cell
  2. express BCR on their cell surface
129
Q

T-cell

A
  1. key component of cell-mediated response
  2. mature in thymus
130
Q

surface receptor of T-cells

A

T-cell receptor (TCR)

131
Q

function of T-cells

A

cytotoxic activity or help the activation of IR

132
Q

diversity of T-cells

A
  1. CD4+ Helper T-cell
  2. CD8+ Cytotoxic T-cell
  3. memory T-cells
133
Q

CD4+ Helper T-cells

A
  1. effector cells
  2. help the activation of the adaptive IS
134
Q

CD8+ Cytotoxic T-cells

A
  1. effector cell
  2. kill infected cells
135
Q

memory T-cells

A
  1. memory cells
  2. express TCR and CD4 or CD8 on their cell surface
136
Q

activation of adaptive IS

A

antigen presenting cells (APCs) such as dendritic cells, that have engulfed pathogens by phagocytosis can present the antigens to naïve CD4+ Helper T-cells (TH)

137
Q

differentiation of adaptive IS

A

depending on type of antigen it encounters, TH cells can differentiate 2 subsets

138
Q

subset to induce humoral immunity

A

activated Th cells can differentiate into a subset called TH2

139
Q

subset to induce cell-mediated immunity

A

activated Th cells will differentiate into a subset called TH1

140
Q

humoral immunity and Th2 cells

A
  1. activated and differentiated Th2 cells activate B-cells and induce their differentiation into plasmocytes
  2. plasmocytes produce antobodies specific for the invading pathogen
141
Q

humoral vs cell-mediated immunity

A

humoral: antibody-mediated response
cell-mediated: cytotoxic-mediated response

142
Q

cell-mediated immunity and Th1 cells

A
  1. activated and differentiated Th1 cells activate CD8+ cytotoxic T-cells and induce their differentiation into CTL
  2. CTL recognize and eliminate any cells displaying the specific antigen presented at their cell surface by MHC class I complex
143
Q

CTL

A

cytotoxic T lymphocyte

144
Q

antibody (immunoglobin or Ab)

A
  1. large Y-shaped protein
  2. each antibody is highly specific and recognizes one epitope
  3. produced by B-cells and exist in 2 forms
145
Q

2 forms of antibodies

A
  1. surface antibodies
  2. soluble antibodies
146
Q

surface antibodies

A

membrane bound on B-cells, forming part of the BCR

147
Q

soluble antibodies

A

secreted by B-cells (plasmocyte) and circulate freely in the blood
- one B-cell will produce one specific antibody for one specific epitope

148
Q

B-cell receptor (BCR)

A

made of a membrane-bound antibody and signal transduction molecules

149
Q

functions of antibodies

A

eliminate a pathogen through various processes

150
Q

processes in which antibodies eliminate a pathogen

A
  1. neutralization
  2. opsonization
  3. complement activation
  4. effector cell activation
151
Q

neutralization

A

neutralize the biological effect of a pathogen or toxin

152
Q

opsonization

A

mark foreign invaders for phagocytosis

153
Q

complement activation

A

induce the formation of membrane attack complexes and opsonization

154
Q

effector cell activation

A

recognized by immune cells when bound to antigen and activate the cell’s effector functions

155
Q

immunoglobins

A

two heterodimeric proteins that are held together by disulfide bones (S-S)

156
Q

heterodimeric

A

protein composed of 2 different polypeptide chains

157
Q

basic structure of human immunoglobins

A
  1. 2 light chains
  2. 2 heavy chains
  3. 2 antigen binding regions
  4. 1 Fc regions (fragment crystallizable)
158
Q

light chain

A

protein subunit that, as one of a pair, forms part of the
main antigen-binding region of an antibody

159
Q

heavy chain

A

protein subunit that makes up the majority
of the structure of the antibody
- forms part of the antigen-binding region and forms the Fc region

160
Q

2 antigen binding regions

A
  1. this region is variable and changes from one antibody to another,
    but remain the same on one antibody
  2. responsible for diversity and specificity of immunoglobins
161
Q

1 Fc regions (fragment crystallizable)

A
  1. is constant for every antibody of the same class
  2. part that interacts with immune cell surface receptors called Fc receptors
162
Q

classes of immunoglobulins

A

5 different classes distinguished by type of heavy chain within their structure
- each type targets a different type of antigen

163
Q

variation in heavy chain polypeptides

A

allows each immunoglobulin class to function in a different type of immune response or during a different stage of the body’s defence response

164
Q

where are the specific amino acid sequences that confer functional differences?

A

mainly within the Fc domain

165
Q

5 different classes of immunoglobulins

A
  1. IgG have y-heavy chains
  2. IgM have u-heavy chains
  3. IgA have a-heavy chains
  4. IgE have e-heavy chains
  5. IgD have 8-heavy chains
166
Q

serum

A

when blood is put into centrifuge, the blood plasma or serum is the liquid that has been separated from the blood cells in whole blood

167
Q

IgM

A
  1. forms a pentamer from IgM monomers when secreted by B-cells
  2. first antibody to be formed in an IR
  3. activated the complement which then amplifies the inflammatory and adaptive IR
168
Q

IgG

A
  1. monomer when secreted by B-cells
  2. coats pathogens to promote phagocytosis and immune cell recruitment
  3. only class that can cross the placental barrier
169
Q

placental barrier

A

the semipermeable layer of tissue in the placenta that serves as a selective membrane to substances passing from maternal to fetal blood

170
Q

IgA

A
  1. generally forms a dimer from IgA monomers when secreted by B-cells
  2. first line of defence and predominant antibody class located in the body’s mucosal membranes (respiratory and gastrointestinal tracts)
171
Q

IgE

A
  1. monomer when secreted by B-cells
  2. found in large quantity on the surfaces of antigen-naive mature B-cells
  3. function or importance is UNCLEAR, thought to have a role during B-cell development
172
Q

Y-chain

A
  1. IgD
  2. IgE
  3. IgG
173
Q

double Y-chain

A

IgA (dimer)

174
Q

5 Y-chains

A

IgM (pentamer)
- form very large antibody molecule

MICR 270 (5 decks)

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