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HE303 - Immunology > Test 1 > Flashcards

Test 1 Flashcards

Lesson 1-4

1
Q

what is immunology?

A
  • the study of the physiological mechanisms that animals use to defend themselves against invasion by other organisms
  • the immune system is what protects us from invading organisms (viruses, parasites, bacteria, fungi) and cancer
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2
Q

what is the purpose of the immune system?

A
  • it recognizes and destroys things that are dangerous to our bodies (dangers) and induce an immune response
  • these dangers can be exogenous or endogenous = varied responses
  • can induce a range of effector responses within the body to remove pathogens and control tumour cells (if we reacted the same way, it wouldn’t be effective)
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3
Q

2 types of dangers

A

1) endogenous
- originate outside the body
- pathogens are microorganisms that cause disease
- examples: viruses, bacteria, parasites, fungi
2) exogenous
- originate inside the body
- examples: damaged cells, cancerous cells

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4
Q

what are the types of “dangers”?

A

1) viruses
2) bacteria
3) fungi
4) parasites
5) tumours
*note: not ALL bacteria and viruses are “dangers”, some are good!

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5
Q

what are viruses?

A
  • an intracellular pathogen
  • they’re small
  • rely on a host cell to get inside and use their cellular machinery to replicate
  • are treated with antivirals (but hard to treat)
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6
Q

what are bacteria?

A
  • an extracellular pathogen
  • do not require host cell because they can replicate on their own
  • can be treated with antibiotics (treated easier because its outside cell)
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7
Q

what are tumours?

A
  • are a group of cells that have lost control of their cell cycle and divide uncontrollably
  • a characteristic of cancer is their ability to evade the immune system
    –> in order for cancer to establish, cells with mutation need to hide from immune system
  • they’re endogenous (self cells that mutate)
  • NOT a pathogen
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8
Q

what is immunity?

A
  • the state of protection against foreign pathogens or substances (antigen)
    –> second exposure to the same pathogen = reduced or no symptoms = immunity
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9
Q

what is an antigen?

A

anything that causes an immune response in your body

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10
Q

how long has immunity been observed?

A
  • dates back over 2000 years
  • Ancient historian Thucydides noticed that people who got the plague didn’t get sick again (they could help those who were actively sick)
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11
Q

why are children more at risk of illness?

A
  • children are disproportionately affected
  • first time being exposed = haven’t developed immunity yet = immune system cannot mount a strong response
  • their system is still immature and hasn’t developed enough memory cells
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12
Q

what are the two arms of the immune system?

A

1) innate (inborn)
2) adaptive (needs to be induced)
–> they work together to eliminate pathogens or tumours
–> adaptive and innate immune systems overlap and contribute to our immmuneness

innate is more important than adaptive

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13
Q

what is the innate immune response?

A
  • every organism has an innate response (animals, plants, bacteria etc)
  • includes barriers (i.e skin, mucus membrane) to form first line of defence
  • also includes phagocytes (macrophages, neutrophils etc) as backup to destroy pathogens if it enters the body
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14
Q

characteristics of the innate immune response

A
  • responses do not change after repeated exposure to the same pathogen or antigen
  • the response is NON-SPECIFIC = activation by one pathogen can provide some immunity against other pathogens
  • also referred to as “broad spectrum” or “cross reactive”
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15
Q

what is the adaptive immune response?

A
  • only present in animals with a backbone and a jaw
  • 3 important characteristics:
    1) Specificity = incredibly specific, combatfs one specific pathogen
    2) Diversity = mounts an immune response to almost anything
    3) Memory = responds to a reinfection faster and stronger than a first exposure (escalating response)
    –> the foundation of vaccines!
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16
Q

how does the adaptive immune response relate to vaccines?

A
  • vaccines aim to “train” and prime the adaptive immune system to recognize and respond more effectively to pathogens without causing the actual disease
    –> 1st vax = first encounter = learns the pathogen = slow response
    –> 2nd vax = responds stronger = better defence
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17
Q

how does a pathogen flow through the body?

A

barrier –> innate –> adaptive
- most pathogens are stopped at barriers as first line of defence
- innate immune response is activated (i.e phagocytes, complement) and is usually sufficient to prevent infection
- if innate immune fails, this leads to the activation of adaptive immunity
- adaptive immunity kicks in to provide a more specialized response (t-cells, b-cells)

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18
Q

why are barriers important?

A
  • they act as the first line of defence against pathogens
  • they prevent pathogens from entering our bodies
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19
Q

what are barriers in the body?

A
  • physical and cellular ways to keep pathogens outside the body

1) skin
2) mucosa
–> lungs, GI tract, genitourinary system

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20
Q

what are the barriers made up of?

A
  • made of epithelial cells that line a body’s surface
  • act as a boundary between the inside of body and the outside environment
  • epithelial cells create their strong barrier using tight junctions
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21
Q

what are epithelial tight junctions?

A
  • tight junctions form between adjacent epithelial cells
  • proteins connect together to make the tight junction stick and seal
  • nothing can move from the apical (outside) to basal (inside) side of the epithelial layer

*when tight junctions are healthy, they prevent pathogen from crossing the epithelial barrier into deeper tissues or the bloodstream
*when tight junctions become leaky and loose, it allows stuff to get into the body that shouldn’t be there!

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22
Q

examples of barrier defenses

A

1) ciliated epithelial cells
- finger like projections that line airways to sweep inhaled pathogens up and out of lung
- mucociliary escalator (works by coughing out mucus)
2) goblet cells
- located in mucosal surfaces that secret mucous containing glycoproteins and enzymes that bind to, trap and digest pathogens
3) surfactant-producing cells
- located in lung and GI tract that secrete surfactant protein that bind to pathogen cell walls to facilitate their destruction by immune cells
- they mark and make it more visible to the immune system
4) mucosal epithelial cells
- transport antibodies from inside the body to the mucosal surface to enable the antibody to bind pathogens

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23
Q

what are surfactant proteins?

A

two groups:
1) surfactant protein A (SP-A)
2) surfactant protein B (SP-B)

–> found in mucus and support barriers
–> they will speicifcally bind pathogens and NOT host cells

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24
Q

role of surfactant proteins

A
  • can bind bacteria and cause lysis (bursting, leak, rupture) directly by creating pores
    OR
  • make bacteria more visible via tagging so the immune system can recognize they’re harmful = phagocytes can engulf and remove them
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25
Q

how do humans make their own antibiotics?

A
  • host cells produce ⍺ and β defensins, which are antimicrobial peptides (AMPs)
  • produced by epithelial cells (and neutrophils)
  • located in mucus to destroy pathogens
  • made by humans, vertebrates, invertebrates, plants an some fungi
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26
Q

how do AMPs work?

A
  • AMPs insert into pathogen cell walls, disrupt membranes, and cause pore formation = leading to cell lysis and death.
  • bacterial cell walls are more negatively charged (-) than host cells, attracting positively charged (+) AMPs.
  • this results in the destruction of the pathogen, protecting the host from infection
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27
Q

what can weaken our bodies barriers?

A
  • barriers are not perfect because we still get sick
  • pathogen can cross barriers because they have mechanisms to get around it
  • we can compromise our barriers (i.e scraped knee, burns)
    –> if our barriers are crossed then our innate immune response steps up
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28
Q

what does it mean that innate immune responses are conserved across multicellular organisms?

A
  • innate responses are present in all multicellular organisms
  • not all have the SAME response or immunity
  • conserved means that our innate response has remained relatively unchanged throughout evolution across different species
    –> for example, NF-κB, a transcription factor used in immune responses, works the same in all eukaryotes
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29
Q

cells of the innate immune system

A
  • white blood cells (also called leukocytes)
  • all leukocytes are innate immune cells EXCEPT lymphocytes
  • lymphocytes, such as b-cells and t-cells are adaptive immune cells
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30
Q

how is the innate immune response initiated?

A
  • some parts of the innate system are always “on” (i.e skin)
  • some parts must be turned on or activated (PRRs, phagocytic cells, complement system)
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31
Q

why would it be bad for the innate system to always be ON?

A
  • it wouldn’t be as effective
  • it would use a lot of the bodies resources
  • could also result in chronic inflammation or autoimmunity
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32
Q

what are receptors in innate immune system?

A
  • called pattern recognition receptors (PRRs)
  • they bind to the structures produced by pathogens (PAMPs) or released by damaged cells (DAMPs)
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33
Q

what are PAMPS and DAMPS?

A

1) PAMP = pathogen associated molecular pattern
- molecules produced by pathogen that isn’t produced by the host cell = indicates something is wrong
2) DAMP = danger associated molecular pattern
- molecules which are usually inside a cell are detected outside a cell
- i.e ATP or heat shock patterns

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34
Q

what is the role of PRRs?

A
  • PRRs recognize PAMPs and DAMPs, indicating something is wrong
  • upon binding, it will initiate an immune response

*the immune system’s response differs for bacteria and viruses based on the types of PAMPs and DAMPs recognized.

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35
Q

cells of the adaptive immune system

A

2 types of cells:
1) T- cells (CD4 and CD8 t-cell)
2) B-cells

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36
Q

role of b-cells and t-cells

A
  • B-cells produce antibodies for a long range, distance site of infection
  • CD4+ t-cell are helper cells that orchestrate an immune response
  • CD8+ t-cell are cytotoxic that move to the infected tissue and physically destroy infected cells
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37
Q

types of receptors in adaptive immune system

A

1) T- cell antigen Receptor (TCR
- found on T cells
2) B-cell antigen Receptor (BCR)
- found on B cells

*the collection of TCRs and BCRs present in your body is your unique repertoire. this can change over time

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38
Q

what is viral load?

A
  • refers to the amount of virus in an infected person’s blood
  • the more pathogens that get into the host cell, the harder it is for a body to fight it
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39
Q

how is the adaptive immune response so diverse?

A
  • lymphocytes (B cells and T cells) can make a diverse number of receptors by changing the organization of its DNA
  • this produces highly variable receptors, allowing them to bind unique ligands (substances)
  • therefore, each b-cell or t-cell could have a unique receptor = more diversity = stronger immune response
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40
Q

what is a ligand?

A

a ligand is a substance that binds to a receptor

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41
Q

how is the adaptive immune response so specific?

A
  • the specific sequence of a receptor determines which ligands (antigen) it can bind
  • allows the adaptive immune system to precisely target pathogens, producing an effective response
  • only the exact match with fit into a receptors binding site
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42
Q

Why is clonal expansion crucial for lymphocytes in responding to pathogens?

A

clonal expansion allows lymphocytes to rapidly increase in number when they recognize a pathogen, enhancing the immune response’s effectiveness against infections.

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43
Q

how does clonal expansion occur?

A
  • b-cells and t-cells make copies of themselves, especially when they are highly effective in combating an infection.
  • one cell wouldn’t be strong enough to fight off a pathogen, so more are required
    1) a repertoire of lymphocytes contain single b and t cells with unique receptors
    2) once that t-cell or b-cell finds its unique match, it undergoes rapid mitosis to make lots of daughter cells (clones)
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44
Q

two phases of adaptive immunity

A

1) primary immune response
- is the first time you are infected with a pathogen
- weaker and slower response
- could be natural or by vaccination
2) secondary immune response
- subsequent reinfection with the same pathogen
- faster, stronger, more robust response
- have already found important cells to fight the infection

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45
Q

What are naive T cells and B cells?

A
  • when a lymphocyte has never been activated and is still searching for its unique antigen
    –> naive t-cells circulate through the bloodstream and move through secondary lymph organs (spleen, lymph nodes) to search for matching antigen
    –> naive b-cells reside in b-cell areas of lymph nodes awaiting their matching antigen and t-cell activation
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46
Q

how do naive cells get activated?

A
  • by searching for their matching antigen
  • once activated, they can do their job and defend infection
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47
Q

what do activated t-cells do?

A

CD4+ helper T cells:
- Help with shaping the immune response
- Help activates B cells

CD8+ killer (cytotoxic) T cells:
- Move to the infected tissue and kill infected cells or cancerous cells

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48
Q

what do activated b-cells do?

A
  • stay in the lymph node and differentiate into plasma cells
  • they’re antibody producing machines
  • they secrete antibodies that are essentially soluble forms of their B cell receptors (BCRs)
  • the antibodies move to the infected area of the body
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49
Q

what is the difference between humoral and cell-mediated immune response?

A

1) humoral response
- involves the production of antibodies by b-cells (b-cells differentiate into plasma cell)
- usually kills extracellular pathogens and toxins

2) cell-mediated response
- involves t-cells that directly attack infected cells or coordinate immune responses
- usually attacks intracellular pathogens and tumour cells

*the response depends on the danger/pathogen we are fighting

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50
Q

What is the duration of the primary immune response and what happens to B and T cells after the infection is cleared?

A
  • it takes 7-10 days for a primary immune response to fully mount
  • this invovles:
    1) cellular activation
    2) proliferation (making clones)
    3) differentiation (b-cell –> plasma cell)
  • after T-cells and antibodies control the infection, 90-95% of activated B and T cells die through apoptosis (programmed cell death).
  • 5-10% remain as memory B and T cells, allowing for a faster response upon future exposure to the same pathogen.
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51
Q

what is the importance of memory cells?

A
  • they set the stage of secondary immune response
  • without memory cells, the response would be the same
  • memory cells mediate a better, faster response for a subsequent infection
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52
Q

what is the secondary immune response?

A
  • occurs after a reinfection with the same pathogen
  • adaptive immune response is already sensitized and will response quicker this time
  • activated memory cells clonal expand and produce a rapid immune response within 2-3 days (versus 7-10 days)
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53
Q

why do memory t-cells activate easier than naive t-cells?

A
  • they’re already located in the past site of infection
  • more likely to “see” the pathogen and turn on readily
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54
Q

what is a vaccination?

A
  • a method to produce immunity in healthy individuals
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55
Q

how do vaccines work?

A
  • the vaccine is either killed pathogen, attenuated pathogen of pieces of a pathogen that induces a primary immune response
  • primary response results in memory b-cells and t-cells
  • this protects us when we’re infected with the actual, live pathogen (gets rid of it faster, or doesn’t allow us to sick at all)
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56
Q

what are adjuvants?

A

the part of the vaccine that triggers the innate immune response so that the body is ready to “see” the vaccine

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57
Q

why are adjuvants necessary in vaccines, and what happens if the innate immune response is not triggered?

A
  • adjuvants provide necessary signals for t-cell and b-cell activation
  • without proper signalling, t-cells and b-cells may ignore the pathogen
  • adjuvants help prevent the development of tolerance to pathogens (ignoring the pathogen)
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58
Q

what is hematopoiesis?

A

is the process of blood cell formation

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59
Q

what is the process of hematopoiesis?

A
  • hematopoietic stem cells (HSC’s) will receive signals to make/stop blood cell production
  • HSC’s give rise to:
    1) myeloid progenitor cells = differentiate into most leukocytes (monocytes, eosinophils, dendritic cells, mast cell, basophils, neutrophils)
    2) lymphoid progenitor cells = develop into lymphocytes = t-cell, b-cell, NK cells
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60
Q

what are Hematopoietic stem cell (HSC)?

A
  • are specialized cells that can self-renew and give rise to any type of blood cell (hematopoietic cells)
  • they are highly responsive to stimuli and rapidly grow to meet the body’s needs
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61
Q

what are progenitors?

A

precursors to mature cells

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62
Q

what are the cells of the immune system?

A

in blood:
- neutrophils
- eosinophils
- basophils
- monocytes
- lymphocytes (b-cell, t-cell, NK cell)

in tissues:
- mast cells
- dendritic cells
- macrophages

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63
Q

what are leukocytes? what are lymphocytes?

A
  • leukocytes are the term for all WBC’s
  • 2 main types: phagocytes and lymphocytes
  • lymphocytes are a type of white blood cell (containing b-cell, t-cell and NK cells)
    –> Thus, all lymphocytes are leukocytes but all leukocytes are not lymphocytes.
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64
Q

what classes of immune cells are found in the blood?

A
  • polymorphonuclear cells (PMNs)
  • peripheral blood mononuclear cells (PBMCs)
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65
Q

what are polymorphonuclear cells?

A

these are all part of the innate immune system
- neutrophils
- eosinophils
- basophils
–> they all contain granules with enzymes that are released to fight infection

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66
Q

what are neutrophils?

A
  • the first leukocyte recruited to sites of infection
  • most common white blood cell (50-70%)
  • multi-lobed nucleus
  • produced in large numbers everyday, but don’t live long
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67
Q

what happens when neutrophils die?

A
  • they release large neutrophil extracellular traps (NETs) composed of DNA fibres coated with pathogen-degrading enzymes
    –> netosis = form sticky nets to immobilize and further break down the pathogen
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68
Q

how do neutrophils stop infection?

A

1) phagocytosis
- surface receptors on the neutrophil recognize the pathogen
- the neutrophil engulfs the pathogen, resulting in death of pathogen and self
2) release reactive oxygen species
- damages pathogen and tissues

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69
Q

what are basophils?

A
  • key role in defence against parasites
  • express high affinity for receptors IgE (their target antigen)
  • rapidly release pre-formed inflamattory cytokines from granules
  • rare
70
Q

what are eosinophils?

A
  • key role in defence against parasites
  • release highly basic and cationic proteins into extracellular space = toxic to pathogens
  • they express pro-inflammatory cytokines that contribute to the immune response
  • NOT phagocytic
  • rarer
71
Q

what are peripheral blood mononuclear cells?

A
  • monocytes (innate immune system)
  • lymphocytes: b-cells, t-cells, natural killer cells (adaptive immune system)
72
Q

what are monocytes?

A
  • constitute 2-12% of the total white blood cell count
  • belong to the innate immune system
  • they enter tissue and differentiate into macrophages
73
Q

what are lymphocytes

A
  • about 20-40% of all white blood cells
  • includes b-cells, t-cells, NK cells
74
Q

what are Tregs?

A
  • a group of CD4 helper t-cells that work to decrease immune response
  • ensures that immune response doesn’t last forever
  • 10% of CD4 t-cell are Tregs
75
Q

what are natural killer (NK) cells?

A
  • are innate cells that can be activated to kill virus infected cells or tumour cells
  • secrete cytokines
  • kills infected/damaged host cell
76
Q

what are the specialized cells of the innate immune system? what is their role?

A
  • phagocytes are the cells of the innate immune system
  • they work after a pathogen bypasses a barrier, such as skin or mucous membrane
  • their primary role is to engulf and destroy pathogens through the process of phagocytosis.
    –> phagocytic cells consist of mostly macrophages and neutrophils
77
Q

what immune cells are found in tissue?

A

belong to the innate immune system
- macrophages
- mast cells
- dendritic cell

78
Q

what are macrophages?

A
  • a large cell that kills pathogens via phagocytosis
  • clean up apoptotic cells and contribute to repair
  • produce pro-inflammatory cytokines
  • act as a APC (antigen presenting cell)
  • they’re relatively long lived (months)
79
Q

what are mast cells?

A
  • cells that contain and release pre-formed inflammatory mediators (i.e histamines, cytokines)
  • express high affinity receptors for IgE
80
Q

what are dendritic cells?

A
  • cell found at all barriers, close to epithelial cells
  • they pick up antigens from tissues and transport them to other areas to initiate the immune response
  • act as antigen presenting cells (APCs) to other immune cells
81
Q

how do dendritic cells contribute to t-cell activation?

A
  • dendritic cells exist in the tissue in an immature state, meaning it can engulf antigens
  • dendritic cells drain from the tissue into lymph nodes, which increase during inflammation
  • as they travel to the lymph nodes, the dendritic cells mature, losing their ability to take up antigens but becoming very effective at presenting antigens
  • mature dendritic cells present antigens to T cells using Major Histocompatibility Complex (MHC) molecules
  • dendritic are the only antigen-presenting cell (APC) that can activate a primary immune response
82
Q

why are dendritic cells important?

A

if no dendritic cell present = no t-cell activation = no adaptive immune response = PROBLEM

83
Q

what are immune mediators?

A
  • are important substances produced and released by cells in the immune system that facilitate effective communication during immune responses
  • a general term for mediator is “cytokines”
84
Q

how do immune mediators work?

A
  • are soluble substances (proteins) released from cells that can travel through the body and are sensed by others cells to their behaviour/response
  • they are called cytokines
  • they can work together to produce inflammatory cascades (tons of signalling)
85
Q

what are characteristics of cytokines?

A
  • PLEIOTROPIC = a single cytokine has multiple actions depending on cell type and pathway
  • REDUNDANT = several cytokines can produce the same response
  • COOPERATIVE = many cytokines are produced together from the same stimulus OR can enhanced the production of other cytokines
  • some can act locally (autocrine = themselves, paracrine = neighbour) or systemically (endocrine)
    –> some can do all of these by starting locally and then sending systemic signals for increased response
86
Q

2 groups of cytokines

A

1) interleukins (IL)
2) chemokines

87
Q

what are interleukin (ILs)?

A

interleukins (ILs) are a type of cytokine
2 types:
- pro- inflammatory
- anti-inflammatory

88
Q

what are chemokines?

A

chemokines are another type of cyokine
- are proteins that causes cells to migrate in a specific direction
-they create a chemokine gradient that cells can follow (move toward higher concentrations of chemokines)

89
Q

What is the mechanism of action of cytokines in the immune response?

A

cytokines act by binding a cytokine receptor on surface of a cell = initiate signalling cascade within cell = produce second messages = activate transcription factors controlling gene expression = produce new proteins with specific roles

90
Q

two types of chemokine expression

A

1) constitutive = always present at low levels
- chemokine expression is crucial for regulating the normal movement of leukocytes to specific tissues

2) induced = must be “turned on”
- in response to inflammation or injury, chemokines are produced in greater amounts, recruiting immune cells to the affected area

91
Q

significance of cytokine signaling and receptor specificity

A
  • cytokines act as signaling molecules that facilitate communication between cells in the immune system
  • not all cell types express all types of cytokine receptors
  • for a cytokine to exert its effects, it must bind to its corresponding receptors on the target cell
92
Q

what happens after a cytokine binds with its receptor?

A
  • the binding of a cytokine with its receptor initiates a signaling cascade within the cell
  • bindings often leads to protein phosphorylation, activating various signalling proteins downstream
  • this leads to activation of specific transcription factors, which move from the cytoplasm into the nucleus
  • in the nucleus, transcription of particular proteins needed for immune response occurs
93
Q

what is cluster of differentiation (CD)?

A

CD = cluster of differentation = a group of cell surface molecules that help us mark and identify what a cell type is within the immune system
–> CD4 vs CD8

94
Q

what parts of your body can get infected?

A

EVERY PART! but certain parts are more likely, but all have risks
–> this means that our immune system must be able to access and respond to infections in every part of the body
–> however, the immune system doesn’t respond the same way in every part of the body (not equal)

95
Q

how does the immune system respond to infections in different parts of the body?

A
  • tissue specific responses = different tissues (gut vs muscle) have unique immune responses
  • immune-privilege tissues = some areas like the eye, placenta, fetus, and CNS, have limited immune responses to prevent damage
  • some immune cells normally reside in tissues
  • some immune cells need to be recruited to the site of infection
96
Q

how do immune cells move through the body?

A

1) blood = blood has access to every organ
2) lymphatic systems = move through lymoh

97
Q

what is lymph?

A
  • protein-rich liquid derived from blood plasma
  • circulates through the lymphatic system
98
Q

what is the lymphatic system?

A

a network of blood vessel that are filled with lymph

99
Q

what is the cycle of the lymphatic system?

A
  • white blood cells (leukocytes) circulate through the lymphatic system
  • lymph drains from tissues and organs into lymphatic vessels
  • from vessels, it drains into lymph nodes
  • after lymph nodes, goes back into the blood
100
Q

how does lymph move through the body?

A
  • lymph does NOT have a pump
  • it moves through a series of one-way valves that keep lymph moving in the right direction
  • lymph moves when we move (i.e active)
    –> sedentary lifestyle = accumulate lymph = detrimental to health
101
Q

what are the primary and second lymphoid organs?

A

1) primary lymphoid organs
- bone marrow and thymus
- sites of leukocyte production and maturation
- where hematopoiesis occurs
2) secondary lymphoid organs
- lymph nodes, spleen, Peyer’s patches, mucosal tissues
- the sites of leukocyte activation

102
Q

what is the importance of the bone marrow?

A
  • bone marrow is the site for hematopoiesis = production of leukocytes (including b-cell, t-cells)
  • has a specialized microenvironment containing stem cells and growth factors
  • bone marrow is the site for B-cell development and maturation
103
Q

what is the selection process of b-cells in the bone marrow?

A
  • pre-B cells produce their B-cell receptor (BCR) through a process of random receptor rearrangement
  • while this process allows for diversity, it can also result in auto-reactive BCRs = bad
  • b-cells undergo negative selection to assess their B cell receptors (BCRs).
  • BCRs that bind to self-antigens (normally found in the body) are called auto-reactive b-cells
  • auto-reactive b-cells are typically eliminated through apoptosis to prevent autoimmunity
  • B-cells that don’t bind to self-antigen receptors on host cells are allowed to differentiate into mature b-cell and go to secondary lymphoid organs
  • b-cells leaving the bone marrow are considered mature but NAIVE = not yet encountered their specific antigen receptor yet
104
Q

what is the importance of the thymus?

A
  • the site of T-cell development and maturation
  • immature t-cells produced in the bone marrow move to the thymus for maturation
105
Q

how does the thymus change throughout your life?

A

–> the thymus very active before birth and during childhood when immune system is being established
–> peaks in size at puberty then dwindles with ages = why older people get sick easier

106
Q

what are antigen-presenting cells (APCs)?

A
  • are immune cells (phagocytes) that have detected and engulfed a pathogen then digested it into various antigen fragments
  • these fragments (proteins) are placed onto MHC class I or MHC class II molecules on the surface of the immune cell
  • the APC may now interact with t-cell receptors (TCRs)
  • this presentation is essential for initiating and coordinating a targeted immune response against the infection.
107
Q

what is the Major Histocompatibility Complex (MHC)?

A
  • MHC is a set of molecules expressed on the surface host cells (typically thymic cells)
  • it presents antigen fragments (proteins)
  • t-cell receptors binding to MHC determine if it can become activated or not
  • without MHC, you wouldn’t activate a single t-cell
108
Q

2 roles of MHC

A

1) helps t-cells determine “self” vs non self by displaying the unique MHC molecules present on your own cells.
–> If cells from another individual are introduced, their different MHC molecules will be recognized as non-self
2) helps t-cells recognize antigens and respond with an immune response
–> T cell receptors (TCRs) cannot recognize free-floating antigens
–> TCRs can only detect antigens presented to them by MHC molecules

109
Q

What are the two stages of t-cell selection, and what is their purpose?

A
  • selection occurs in the thymus
  • it is a dual-selection process that decides of a t-cell lives or dies
  • t-cells begin by making their t-cell receptors (TCRs) and then will test to see if their TCRs can bind major histocompatibility complex (MHC) of self thymic cells
    1) positive selection = allow t-cells that recognize and moderately bind their TCR to self-MHC to survive
    –> they can recognize self = good
    2) negative selection = eliminates t-cells that bind their TCR too strongly to MHC-peptides complexes on self cells are deleted by apoptosis
  • if the t-cell pass their selection processes they move to the secondary lymphoid organs.
110
Q

what are the two MHC classes?

A

1) MHC Class I
- found on every nucleated cell
- activates CD8+ cytotoxic T cells and their downstream effects
- involved in presenting antigens from intracellular sources
2) MHC Class II
- presented by only antigen-presenting cells (APCs) and activated t-cells
- involved in presenting antigens from extracellular pathogens
- activates helper CD4 t-cells and their downstream effects

111
Q

how do APCs present pathogens using MHC Class II molecules?

A
  • they ingest extracellular pathogens, such as bacteria, through a process called phagocytosis
  • once inside the APC, the pathogens are chopped into smaller antigen fragments (proteins)
  • these fragments are then loaded onto MHC Class II molecules
  • the MHC Class II-peptide complex is displayed on the surface of the APC, where it can be recognized by CD4+ T helper cells
  • this interaction is crucial for activating t-cells and adaptive immune response
112
Q

what would happen without t-cell selection in the thymus?

A

without maturation in thymus, the body would be deficient in t-cells and lead to inability to fight infections
1) immune deficiency
- without positive selection, T cells that cannot recognize self-MHC molecules would not be removed = would be unable to recognize and respond to antigens = ineffective immune response
2) autoimmunity
- if negative selection didn’t occur, T cells that bind too strongly to self-antigens would not be eliminated = self-reactive T cells could attack the body’s own tissues, leading to autoimmune diseases.

113
Q

what are the secondary lymphoid organs?

A

1) lymph nodes
2) spleen
3) mucosa-associated lymphoid organs (MALT)
–> promote adaptive immune responses

114
Q

How do antigens move through the lymphatic system and facilitate activation of T and B cells?

A
  • antigens are funneled from tissues into secondary lymphoid organs, where they interact with t-cells and b-cells
  • antigens are compartmentalized/concentrated into certain areas of the lymphoid organ
  • this increases the opportunity for an antigen match with its T cell receptors (TCR) or B cell receptors (BCR)
  • if there was constant circulation there may never be a match for the lymphocytes
  • if any lymphocytes have TCRs or BCRs that recognize the antigen, they become activated
  • a match mean the antigen matches the shape of the receptor on the b-cell or t-cell
  • activated lymphocytes undergo clonal expansion and maturation = ultimately helps destroy the pathogen
115
Q

what happens to t-cells in lymph nodes?

A
  • t-cells are highly mobile (move between the blood + lymph node) to help find their match
  • activated/matched CD4+ t-cells interact with b-cells in the lymph node to activate them
  • activated/matched CD8+ t-cells leave the node and go to site of infection
  • t-cells that do not immediately find their match leave the node through efferent vessels and back through blood
116
Q

what happens to b-cells in lymph nodes?

A
  • b-cells stay put (aren’t mobile)
  • b-cells stays in the node and waits for a antigen to flow in and match its BCR
  • if an antigen flows in and successfully matches its BCR, they receive a 2nd and 3rd signal (from CD4 t-cells and other immune cells)
  • this causes b-cell clonal expansion and maturation
  • b-cells become plasma cells that produce soluble BCRs = antibodies
  • antibodies leave the node, circulate, through body, enter site of infection and help fight
117
Q

what is the role of the spleen as a secondary lymphoid organ?

A
  • spleen only filters antigens out of the bloodstream
  • structurally, the spleen is similar to a massive lymph node
  • t-cells and b-cells reside in a specialized area called white pulp, where antigens can be presented to their BCR and TCR
118
Q

what is the role of Mucosa-Associated Lymphoid Tissue (MALT) in the immune system?

A
  • they contain specialized M-cells which are thin epithelial cells that help facilitate the entry of pathogens through the barrier and into the tissue
    –> typically don’t want direct entry but were funnelling right to the immune system to mount big defence
  • MALT have organized t-cell and b-cell areas to facilitate their activation by antigens
  • when b-cells in MALT are activated and differentiate into plasma cells, they release their antibodies which are released back to the lumen to pathogen entry through the membrane
  • Antigen-presenting cells (APCs) and activated lymphocytes (t-cells and b-cells) can migrate from MALT to nearby lymph nodes = broader and more systemic immune response when needed
119
Q

two theories of how the immune system determines what to respond to

A

1) self/non self model
- Charles Janeway
- the immune system responds to things that are different/foreign like pathogens or transplants
- a fetus is non-self but its not rejected
2) danger model
- Polly Matzinger
- the immune system doesn’t respond to self and non-self, but rather between things that cause damage and things that do not

120
Q

how do the innate cells recognize pathogens?

A
  • they exploit differences between the host cell and pathogen to differentiate them

example: an innate receptor could determine if their is nucleic acid located in the wrong spot
–> DNA in cytoplasm = good indicator of virus
–> DNA in nucleus = bad indicator of virus (because thats where DNA should be)

121
Q

how do immune cells recognize pathogens?

A
  • they use receptors (PRRs) to recognize pathogens, signs of cancer or other damage
  • receptors –> bind ligands –> stimulate signalling pathway = immune response
122
Q

what are receptors of the innate immune system called?

A

called Pattern Recognition Receptors (PRRs)

123
Q

what are PRR’s?

A
  • they are highly diverse group of receptors that recognize and bind to PAMP and DAMP ligands
  • PRRs can be membrane bound, intracellular, or secreted
  • PRRs are distributed everywhere in the body and are capable of sensing pathogens both inside and outside cells
124
Q

what do PRR’s bind to?

A
  • PAMPS (Pathogen Associated Molecular Patterns) = pathogens
  • DAMPS (Danger Associated Molecular
    Patterns) = dangers
    –> PAMPS are structural elements unique to pathogens that aren’t found on host cells
    –> DAMPS are molecules released from damaged or dying host cells associated with cell damage/inflammation
125
Q

what happens when PRRs are activated?

A
  • once it binds a PAMP, it leads to a signalling cascade leading to activation of transcription factors and changes to protein synthesis within the nucleus
  • results in up-regulation of genes associated with:
  • inflammation
  • anti-pathogen responses
  • tissue repair
  • generation of adaptive immune responses
126
Q

what are the classes of innate immune system receptors?

A

1) soluble PRR’s = bind extracellular pathogens
- soluble PRRs are not attached to anything, free floating
- collectins and pentraxins

2) membrane-bound PRRs = bind intracellular
- attached to the membrane
- C-type lectin receptors and TLRs/RLRs/NLRs

127
Q

what is the purpose of soluble PRRs?

A
  • to bind conserved molecular structures on the surface of extracellular pathogens (PAMPS)
  • by binding, it helps carry out opsonization by coating the pathogen for better recognition = enhance phagocytosis
128
Q

what is opsonization?

A
  • a common effector response for the immune system
  • is the process of coating the pathogen with a host protein, called opsonins, such as soluble PRRs or C3b (from complement)
  • this makes the pathogen more visible to phagocytes
  • phagocytes have specific receptors that recognize and bind to the opsonins, which causes engulfing and destruction of pathogens
129
Q

what are the simplified steps of opsonization between antibodies and pathogens?

A

1) antibodies bind to specific antigens on the pathogen’s surface
2) this binding marks the pathogen for recognition by phagocytes, for phagocytosis
3) Antibodies are still bound to the pathogen. The antibody binds to phagocytes receptors on its surface, and attach
4) The phagocyte engulfs the opsonized pathogen, and destroyed within the phagocyte

130
Q

what are the function of membrane bound PRRs

A
  • mediate phagocytosis (c-type lectin receptors)
  • mediate cell signalling (toll-like receptors)
131
Q

what are toll-like receptors (TLRs)?

A
  • a type of membrane-bound PRR
  • every cell expresses some TLRs because it allows cells to detect infections or nearby pathogens
  • have highly DIVERSE ligands they can bind to
  • TLRs are membrane-bound PRRs with two major domains:
    1) one for recognition
    2) one for signalling
132
Q

why is it important for TLRs to have highly diverse ligands?

A
  • each TLR is specialized to recognize specific PAMPs
  • this diversity is essential for the innate immune system to detect a wide variety of pathogens
  • the activation of different TLRs can start a unique signalling cascade to initiate an appropriate response
133
Q

what is an inflammasome?

A
  • a inflammatory response activated by NLRs (Nod-like receptors)
  • an inflammasome is set of receptors in the cytoplasm that regulate and activate an enzyme called of caspase-1
  • caspase-1 is an enzyme that cleaves (cuts) into and activates IL-1β, a pro-inflammatory cytokine
134
Q

what are the 2 signals for inflammasome formation? why 2 signals?

A
  • when activated, it produces a very ROBUST response so 2 signals are needed to control it so it doesn’t mistakingly set off

signal 1:
- the NLR binds to a PAMP and triggers productions of cytokines and another PRR, called NLRP3
signal 2:
- NLRP3 are activated by an influx of ligands = and triggers inflammasome formation

135
Q

what is the complete pathway for inflammasome formation?

A

1) signal 1: PRR binds to PAMP and triggers production of cytokines and another PRR called NLRP3 (a receptor)
2) signal 2: NLRP3 is activated by ligand influx into the cell and triggers inflammasome production
3) caspase-1 in NLRP3 is activated and cleaves into 2 cytokines into their active forms to activate the adaptive immune system
4) these cytokines activate robust inflammatory responses and pyropoptosis (programmed cell death)
–> pyropoptosis acts to kill infected cells by releasing their DAMPS and causing extensive damage

136
Q

what are the outcomes of PRR activation?

A

*not all PRRs signal and create a cascade, but the ones that do:
1) produce type 1 interferons (IFN) = antiviral state (ready to defend)
2) produce pro-inflammatory cytokines = inflammation

–> soluble PRR’s do not signal

137
Q

what is the type I IFN (interferon) pathway?

A
  • the IFN binds to a membrane-bound PRR on host cell
  • type 1 IFN pathways activate transcription factors that lead to production of interferon-stimulated genes (ISGs) within the nucleus of host cell
  • ISGs accumulate within the cell and establish an antiviral state = ready to defend an infection when required

–> this signalling by IFNs can be autocrine (signal to self) or paracrine (signal to neighbour cells)

138
Q

what are the roles of ISGs (interferon stimulated genes)?

A
  • ISGs aren’t active all the time, they wait for an infection
  • they are “stockpiled” within the cell, ready to be activated upon infection
  • ISG’s do the stopping and fight the pathogen

1) PKR blocks protein translation within the cell so virus cannot replicate
2) OAS blocks protein translation too
3) Mx directly blocks virus assembly by preventing it from putting itself together

139
Q

what is inflammation?

A
  • a physiological response to injury or infection
  • inflammation leads to resolution of an infection and tissue
140
Q

what is the purpose of inflammation?

A
  • recruit leukocytes to the site of infection
  • recruit mediators (cytokines) to the site of infection
  • raise body temperature to cause fever and slow down pathogen replication
    –> the recruited cells and mediators will recognize and destroy invading pathogens and contribute to tissue repair
141
Q

3 types of inflammation

A

1) acute local inflammation
2) acute systemic inflammation
3) chronic inflammation (BAD)

142
Q

characteristics of acute,local inflammation

A
  • damage or infection is contained to 1 area
  • vasodilation to increase blood flow to site of inflammation
  • increased vascular permeability to allow cells and proteins into tissue
  • increased migration of leukocytes (neutrophils + phagocytic cells) to inflamed tissue
  • pro-inflammatory cytokines are secreted to promote inflammation and activate recruited leukocytes for phagocytosis
143
Q

characteristics of acute, systemic inflammation

A
  • cytokines act on the hypothalamus, inducing increased body temp and fever
  • cytokines promote production of more leukocytes in the bone marrow to increase number of cells to fight, to replace ones being used up
  • cytokines stimulate the liver to produce acute phase proteins (APPs) such as collectins and pentraxins that help with recognition and destruction of pathogens
144
Q

characteristics of chronic inflammation

A
  • result of acute inflammation that fails to remove the inflammatory stimulant (pathogen/damage)
  • characterized by the continuous presence of activated macrophages that excessively release pro-inflammatory cytokines = increasing inflammatory response
  • causes excessive repair and development of tissue, such as fibrosis = loss of tissue structure
145
Q

what are the innate mechanisms for extracellular pathogens

A

1) phagocytosis = eat pathogen
2) complement activation

146
Q

how do you handle an intracellular pathogen?

A

1) NK-cells
2) Type 1 IFN response

  • the only way is to shut down intracellular pathogens is to kill the whole infected cell because they have a cell membrane to protect them from phagocytes and soluble proteins
147
Q

two classes of phagocytes

A

1) macrophages
2) neutrophils
–> dendritic cells are phagocytes but their purpose isn’t to control infection, the sample pathogens to get antigen for t-cells

148
Q

steps to phagocytic mechanism

A

1) phagocytes recognize pathogens using using surface receptors (PRRs) to bind PAMPS, or self-molecules (i.e complement proteins)
2) the phagocyte changes its shape after biding to the pathogen and wraps around it
3) the phagocyte fuses membranes with the plasma membrane of the pathogen to form an endocytic vesicle, called a phagosome
4) once the phagosome has been fully engulfed and brought into the cell, the phagosome binds with a lysosome to form a phagolysosome
5) the phaygolysosome contains enzymes and antimicrobial peptides that digest and destroy the pathogen
6) the products of the killed pathogen are released from the cell

*if the pathogen isn’t successfully killed, it stays in the cell and affects it

149
Q

why are diverse mediators good for phagocytosis?

A
  • allows for killing of numerous different pathogen
  • BROAD response
150
Q

what is the complement system?

A
  • one of the major mechanisms of the innate immune system that coverts pathogen recognition into immune response
  • is a series of plasma proteins that act together in a cascade to generates various effector functions in the immune system (inflammation, opsonization, lysis)
151
Q

what are the 3 complement pathways?

A

1) classical pathway
2) lectin pathway
3) alternative pathway
–> they have different ways of activating the cascade but have same outcomes

152
Q

what are the 3 outcomes of the complement system?

A

1) LYSIS = create pore in cell walls and membrane attack complex (MAC)
2) INFLAMMATION = promote inflammation and chemo-attract other immune cells
3) OPSONIZATION = coating the pathogen and enhanced phagocytosis

153
Q

how does the beginning of each pathway differ?

A

–> the initiation is different between pathways, but the rest is the same
- alternative pathway = spontaneous hydrolysis of C3
- lectin pathway = lectin PRR binds sugars on pathogen cell walls (PAMP)
- classical = antigen-antibody immune complexes

154
Q

key points of complement systems

A
  • all complement proteins exist as inactive precursors until cleaved
  • there are 3 distinct phases of complement activation
  • complement activation releases anaphylatoxins that stimulate inflammation
  • pathogens coated in complement proteins are more susceptible to phagocytosis
155
Q

what are the 3 steps in the complement system’s response to a pathogen?

A

1) initiation = varies by each pathway
2) amplification = make as much C3 convertase and C5 convertase as possible so it can cleave C3 and C5 into their active forms
3) termination = inflammation, lysis + MAC formation, opsonization + phagocytosis

156
Q

what occurs in the amplification phase of ALL complement pathways?

A
  • C3 convertase cleaves C3 into C3a and C3b.
  • C5 convertase cleaves C5 into C5a and C5b.
157
Q

what are the roles of complement proteins?

A

C3a = lead to inflammation
C3b = opsonization
C5a = lead to inflammation
C5b = lead to lysis and MAC formation

158
Q

what are the functions of C3b and C5b?

A
  • C3b acts as an opsonin, which is a complement protein to coat pathogens to enhance phagocytosis
  • C5b recruits and bins C6,C7,C8,C9 to form a membrane attack protein (MAC) in order to carry out lysis of a pathogen
159
Q

what is the importance of C9 in the complement pathway?

A
  • after C9 is recruited to C5b, it polymerizes to complete the formation of the membrane attack complex (MAC)
  • a pore can form on invading pathogens, and leading to their death
    –> if C9 wasn’t recruited, we couldn’t form a pore for the lysis
160
Q

what are anaphylatoxins?

A
  • C3a, C4a, and C5a are all known as anaphylatoxins
  • they are the small pieces that are cleaved and act as inflammatory mediators
  • they promote inflammation by increasing vascular permeability, promoting chemotaxis of phagocytes to areas of infection and stimulate mast cell degranulation
161
Q

what is enhanced phagocytosis?

A
  • C3b formed from complement act as opsonins to coat pathogen cell walls
  • in order for phagocytes to recognize and engulf the pathogen, they need to recognize the protein
  • the phagocytes express specific complement receptors that bind to C3b on the surface of the pathogen
  • therefore, they can successful recognize the pathogen and the phagocyte can engulf and kill it
162
Q

how is complement regulated?

A

*if complement isn’t tightly regulated than it can cause severe damage
- complement proteins exist as inactive precursors (only active upon cleavage)
- they work in a cascade where one thing actives another = multiple control points
- regulators of complement activation (RCA) and complement control proteins (CCP) block various stages of the pathways to prevent overactivation
- host cells make regularly proteins to “kick” complement proteins off host cells to precent unintended damage

163
Q

what are the innate mechanisms for intracellular pathogens

A

1) natural killer (NK) cells = destroy infected host cell
2) type I IFNs = protect host cell

164
Q

what are natural killer (NK) cells?

A
  • they kill virus infected cells and tumour cells (only the ones that need to be killed)
  • they form the second line of defence against viruses after interferon response
165
Q

what are the 3 steps to NK killing mechanism

A

1) activation
2) recognition
3) killing

166
Q

steps to activation of NK cell mechanism

A
  • activated by cytokines
    –> type I and type II IFNs
    –> pro-inflammtory cytokines
167
Q

steps to recognition of NK cell mechanism

A
  • NK cells do not have antigen receptors like t-cells
  • they recognize which cell to kill based on what the host cell puts on their surface
    –> host cell can put inhibitor ligands = dont kill me, im healthy
    –> host cells can put activating ligands on surface = kill me, i’m infected
  • NK cells have inhibitory and activating receptors that can bind to the presented ligands on host cell = depending on ratio they decide to kill or keep cell (balanced signal model)
168
Q

steps to killing of NK cell mechanism

A
  • killing is based off a ratio of inhibitory/ activatory ligands presented by the host cell
    –> activatory > inhibitory = kill
    –> activatory < inhibitory = don’t kill
  • NK cells induce apoptosis in infected cell using two possible methods

more (-) = don’t kill
more (+) = kill

169
Q

how do NK cells determine whether to kill a host cell based on the presence or absence of MHC Class I molecules?

A
  • MHC Class I are inhibitory signals (don’t kill me!)
  • NK cells determine whether to kill a host cell based on the presence or absence of MHC Class I
  • every cell has MHC Class I that presents viral antigens to t-cells
  • however, viruses can cause infected cells to down-regulate or remove MHC Class I = prevent CD8+ cytotoxic T cells from recognizing the infection and
  • if host cell doen’t present MHC Class I = acts as an activating signal for NK cells to recognize and kill the infected host cell
  • if a host cell displays MHC Class I on its surface = don’t kill
170
Q

2 methods of NK cell killing mechanism

A

these occur simulatenously, but only one cell killed at a time

1) granule exocytosis
- NK cell granules contain granzymes and performin
- they’re pushed into synpase
- performin = poke holes in membrane
- granzymes = activate apoptosis

2) receptor-mediated apoptosis
- all cells express “death receptors” which can trigger apoptosis when activated
- NK cells express “death ligands” that can bind to the receptor
- interaction between receptor and ligand leads to apoptosis

171
Q

what is the type I interferon response?

A
  • IFNs can induce antiviral autocrine (self) and paracrine (neighbour cell) responses
  • IFNs trigger the accumulation of ISGs and establihs an antiviral state
172
Q

what are the roles of interferon stimulating genes (ISGs)?

A
  • reduce viral and host cell DNA replication and protein synthesis
  • produce restriction factors that interfere with the viral life cycle
  • up-regulate MHC Class I and antigen processing pathways to support adaptive immune system
  • up-regulate pro-inflammatory cytokines and activation of immune effectors
  • identify infected cell and trigger apoptosis in the cell

HE303 - Immunology (8 decks)

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