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PABI 6100 Immunobiology > 1. Overview of the Immune System > Flashcards

1. Overview of the Immune System Flashcards

1
Q

Where did the field of immunology grow from?

A
  • observations that those who recovered from certain infectious diseases were then protected from the disease
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2
Q

What is immunity?

A
  • state of protection from infectious disease
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3
Q

What was the earliest reference to immunity?

A
  • those who recovered from plague could safely nurse the currently ill
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4
Q

What was the first recorded attempt to induce immunity?

A
  • dried crusts from smallpox pustules were inhaled/ inserted into small cuts in the skin (variolation) > to prevent smallpox
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5
Q

How was the first vaccine developed?

A
  • Edward Jenner observed that milkmaids who contracted cowpox were then immune to smallpox
  • He reasoned that introducing fluid from a cowpox pustule could protect people from smallpox
  • Inoculated 8 yr old boy with cowpox (to protect against smallpox)/ intentionally infected with cowpox > child did not develop smallpox
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6
Q

How was the induction of immunity to cholera developed?

A
  • Pasteur grew the bacteria that causes fatal fowl cholera in culture
  • Injected chickens with old bacterial culture > became ill but recovered
  • Tested fresh bacterial culture on both previously exposed/ unexposed chickens > chickens with past exposure to old bacterial culture protected from disease/ only previously unexposed chickens died
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7
Q

What was the significance of Pasteur’s work with fowl cholera?

A
  • aging had weakened the virulence of the bacterial pathogen
  • this attenuated strain could be administered to provide immunity against the disease > called it a vaccine
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8
Q

What other vaccines did Pasteur develop?

A
  • vaccinated sheep with anthrax bacteria attenuated by heat treatment
  • first human vaccine with a series of attenuated rabies virus
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9
Q

What is the goal of vaccination?

A
  • to expose individuals to a pathogen in a safe way > allowing immune cells to respond/ develop strategy to fight the pathogen
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10
Q

What infectious disease was successfully eradicated?

A
  • smallpox was eradicated by universal vaccination
  • problem: end of universal vaccination (↑ # of people with no immunity over time) > smallpox is now considered a potential bioterrorism threat
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11
Q

What are some goals of immunology research?

A
  • not only the eradication of infectious disease through vaccination
  • manipulate immune response > treatments to boost/ inhibit/ redirect immune cells (autoimmune disease/ cancer/ allergies)
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12
Q

What does the humoral branch of the immune system involve?

A
  • B cells interact with foreign proteins (antigens) via BCRs
  • differentiate into antibody-secreting (plasma) cells
  • secreted antibodies bind to antigen > help clear from body
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13
Q

What does the cell-mediated (cellular) branch of the immune system involve?

A
  • CD4+ T-helper cells interact with antigen > cytokine secretion (soluble messengers that direct cells of immune system)
  • CD8+ Cytotoxic-T cells interact with antigen > killing of infected cells
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14
Q

What was the first evidence of the humoral response?

A
  • serum from animals immunized with diphtheria can transfer immune state to unimmunized animals
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15
Q

What was the first evidence of the cellular/ cell-mediated response?

A
  • certain WBCs termed “phagocytes” ingested foreign material
  • more active in immunized animals > major effectors of immunity
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16
Q

Who won the 2018 nobel prize in physiology/ medicine?

A
  • James Allison/ Tasuku Honjo > cancer therapy by inhibition of negative immune regulation
  • PD-1/ CTLA-4 = T-cell breaks that inhibit T-cell activation
  • antibodies against PD-1/ CTLA-4 block the breaks > T cell activation
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17
Q

What are the 4 main differences between innate/ adaptive immunity?

A
  • response time: minutes/ hours vs days
  • specificity: limited/ fixed vs highly diverse/ adapts to improve
  • response to repeat infection: same vs more rapid/ effective
  • major components: barriers/ phagocytes/ PRRs vs T/B cells
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18
Q

How do the innate/ adaptive responses work cooperatively?

A
  • activation of innate response > produces signals required to stimulate/ direct behaviour of adaptive immunity
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19
Q

What is hematopoiesis?

A
  • process by which HSCs differentiate into mature blood cells
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20
Q

What is the site of hematopoiesis?

A
  • site shifts during fetal development (starts in yolk sac)
  • ultimately seed in bone marrow at late stages of fetal development
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21
Q

What are 4 major properties of HSCs?

A
  • give rise to all types of blood cells
  • rare > less than 1/ 50,000 of cells in bone marrow
  • most are quiescent under normal homeostatic conditions (only a few divide)
  • self-renewing (some daughter cells retain stem cell characteristics)
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22
Q

What is the fate of dividing HSCs?

A
  • self renew > some daughter cells retain stem cell characteristics
  • daughter cells can differentiate into progenitor cells
  • progenitor cells lose their self-renewal capacity > become progressively more committed to a particular blood cell lineage
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23
Q

What do self-renewing HSCs differentiate into?

A
  • CMP = Myeloid Progenitor Cell
    > gives rise to RBCs/ platelets/ granulocytes/ monocytes/ macrophages/ some DCs
  • CLP = Lymphoid Progenitor Cell
    > gives rise to B and T lymphocytes/ ILCs/ some DCs
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24
Q

What is the role of RBCs? (erythrocytes)

A
  • main function is gas exchange
  • bind antibody complexes for clearance by macrophages
  • can generate compounds like nitric oxide that damage microbes
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25
Q

What is the role of platelets?

A
  • derived from megakaryocytes that reside in bone marrow
  • circulate in blood > participate in blood clot formation
  • clots prevent blood loss/ provide barrier against pathogen invasion
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26
Q

What are the members of the innate immune system?

A
  • granulocytes (neutrophils/ eosinophils/ basophils/ mast cells)
  • monocytes/ macrophages/ some DCs
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27
Q

What are the granulocytes named after?

A
  • named for the densely staining granules in their cytoplasm
  • Neutrophils/ Eosinophils/ Basophils/ Mast cells
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28
Q

How can the granulocytes be distinguished under the microscope?

A
  • different staining properties of granules in standard H&E staining
    > neutrophil granules stain neutral pink
    > eosinophil granules stain brilliant pink
    > basophil granules stain blue
  • neutrophils have multilobed nucleus
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29
Q

What is the most abundant blood cell?

A

RBCs

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30
Q

What are the majority of circulating leukocytes (WBCs)?

A

Neutrophils (50-70%)

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31
Q

What is the main cellular component of pus?

A

Neutrophils

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32
Q

What is used medically as an indication of infection?

A

Leukocytosis
- transient increase in # of circulating neutrophils

33
Q

What is the role of neutrophils?

A
  • swarm to infection site in response to inflammatory molecules
  • phagocytosis
  • secrete antimicrobial and tissue-remodeling molecules
34
Q

What is the role of eosinophils?

A
  • coordinate defence against parasitic organisms, including helminths (parasitic worms)
    > cluster around worms/ damage membranes by releasing granule contents
35
Q

What is the role of basophils?
- non-phagocytic

A
  • Histamine in basophil granules ↑ blood vessel permeability/ ↑ smooth muscle activity > allows immune cells to access infection site
  • response to parasites (helminths)
  • allergy symptoms
36
Q

What are the 3 main functions of proteins in granulocyte granules?

A
  • damage pathogens directly
    > defensins (antimicrobial protein in neutrophils)
  • regulate trafficking and activity of other WBCs
    > RANTES (chemokine in eosinophils)
    > IL-4 (cytokine in basophils/ mast cells)
  • contribute to tissue remodelling at infection site
    > collagenase (protease in neutrophils)
37
Q

What are the professional APCs?

A

monocytes/ macrophages/ DCs

37
Q

What happens when pAPCs encounter pathogens? (3x)

A
  • secrete proteins that attract/ activate other immune cells
  • internalize pathogens via phagocytosis > digest pathogenic proteins into peptides > present them to T cells via MHC II = antigen presentation
  • upregulate costimulatory molecules required for T cell activation
38
Q

What are the 2 broad categories of monocytes?

A
  • Inflammatory monocytes
    > enter tissues in response to infection
  • Patrolling monocytes
    > crawl along blood vessels monitoring repair
    > provide reservoir for tissue-resident monocytes
39
Q

What is the role of macrophages?
- monocytes that migrate to tissues can differentiate > macrophages

A
  • dual role in immune response
    > contribute directly to clearance of pathogens via phagocytosis
    > act as pAPCs
40
Q

Where do most tissue-resident macrophages arise from?

A
  • most arise early in life from embryonic cells rather than from circulating monocytes
    > these can self-renew/ assume tissue-specific functions
41
Q

What are some examples of tissue-specific macrophages?
- all macrophages so phagocytic cells

A
  • microglia in brain
  • kupffer cell in liver
  • langerhans cell in skin
  • subcapsular sinus macrophage in lymph nodes
42
Q

What is the role of DCs?

A
  • arise from both myeloid and lymphoid lineages of HSCs
  • immature DCs capture antigens > process them > migrate to lymph nodes for antigen presentation to naive T cells
43
Q

Since B/T lymphocytes appear identical under a microscope, how can they be differentiated?

A
  • lymphocytes express different CD surface proteins
    > markers used to differentiate lymphocyte subpopulations (B cell/ Th cell/ Tc cell/ ILC-includes NK cells)
44
Q

Why do plasma cells have a large cytoplasm/ lots of ER/ golgi?

A
  • make antibodies (need organelles to make protein)
45
Q

What is the role of activated B cells? (3x)

A
  • can act as pAPCs
  • differentiate into plasma/ memory cells
  • express costimulatory molecules required to activate T cells
46
Q

How many BCRs does each B cell express?

A
  • each B cell expresses a BCR (surface immunoglobulin) with unique specificity
  • each of 150,000- 300,000 BCRs on B cell has identical binding sites for antigen
47
Q

What is the role of plasma cells?

A
  • lose expression of surface immunoglobulin (BCR)
  • become highly specialized for antibody secretion
    > each plasma cell secretes 100’s-1000’s of antibodies per second
48
Q

What are the 2 major types of T cells?

A

Th cell- CD4+ T cells recognize antigen in complex with MHC II
Tc cell- CD8+ T cells recognize antigen in complex with MHC I

49
Q

What happens when naive CD8+ Tc cells bind to MHC peptide complex?

A
  • become activated/ proliferate/ differentiate into CTLs
  • CTLs kill cells that display non-self antigen complexed with MHC I
50
Q

What happens when naive CD4+ Th cells bind to MHC II peptide complex?

A
  • become activated/ proliferate/ differentiate into effector T cell subset
    > Th1/ Th17 > response to intracellular pathogens
    > Th2/ Tfh > response to extracellular pathogens
    > Treg > quell autoreactive responses/ limit normal T cell responses
51
Q

How do NK cells work?

A
  • express receptors for self MHC I > inhibits ability to kill
    > when encounter cells that lost their MHC I > inhibiting receptor no longer engaged > release cytotoxic granules killing target cell
  • express FcRs > link to antibodies specific for pathogenic proteins
    > brings NK cell in contact with target cell > releases granules to kill
52
Q

Where do immune cells develop?

A
  • Primary lymphoid organs
    > Bone marrow/ Thymus
53
Q

Where is the immune response initiated?

A
  • Secondary lymphoid organs
    > LNs/ Spleen/ MALT (tonsils/ appendix/ peyers patches ext)
54
Q

How does the stem cell niche in the bone marrow support hematopoiesis?

A
  • Perivascular niche > lines the blood vessels
    > quiescent long-lived HSCs nurtured by perivascular/ endothelial cells
    > some HSCs divide/ differentiate > myeloid/ lymphoid lineages
  • Endosteal niche > lines the bone
    > osteoblasts regulate the differentiation of lymphoid cells
55
Q

What are the most active sites of hematopoiesis?

A
  • Femur/ Humerus/ Ileum/ Sternum (flat bones)
56
Q

Where do B cells develop?

A
  • B cell progenitors in endosteal niche in association with osteoblasts
  • more mature B cells in central sinuses of bone marrow
    > exit to complete maturation in the spleen
57
Q

Where do T cells develop?

A
  • initially develop in bone marrow
  • migrate to thymus to achieve full maturity
58
Q

How do T cells develop?

A
  • T cell progenitors exit bone marrow at very immature stage > complete development in thymus
  • enter thymus in blood vessels at the corticomedullary junction
    > double negative DN (neither CD4/ CD8 markers)
  • DN cells travel to subcapsular cortex > proliferate
  • travel to cortex > where first express mature TCRs/ interact with cTECs
    > upregulate both CD4/ CD8 > become double positive DP
  • DP cells tested for ability of TCRs to bind MHC-peptide complexes on cTECs > positive/ negative selection
  • positively selected DP thymocytes mature/ lose a marker > become single positive SP
    > migrate to thymic medulla where they encounter mTECs
  • mature SP cells exit thymus via blood vessel of corticomedullary junction (as entered)
59
Q

What is positive/ negative selection?

A
  • DP cells in cortex tested for ability of TCRs to bind MHC-peptide complexes on cTECs (cortical thymic epithelial cells)
    > negative selection > bind with too high affinity (self-reactive) > induced to die
    > positive selection > bind with intermediate affinity > survive
60
Q

What happens in the thymic medulla?

A
  • SP thymocytes encounter mTECs (medullary thymic epithelial cells)
  • mTECs express proteins otherwise exclusively found in other organs
    > negatively select autoreactive T cells not deleted in cortex
61
Q

What happens in secondary lymphoid organs?

A
  • lymphocytes encounter antigen > become activated > undergo clonal expansion/ differentiate into effector cells
62
Q

What are 3 key features of SLOs? (secondary lymphoid organs)

A
  • have anatomically distinct regions of B/ T cell activity
  • develop lymphoid follicles
  • connected via blood/ lymphatic circulatory systems
63
Q

What are lymphoid follicles?

A
  • areas in SLOs for selection of B cells that produce high-affinity antibodies
64
Q

What is the lymphatic system?

A
  • network of vessels with a major role in immune cell trafficking
  • lymphatic vessels filled with lymph derived from blood plasma that seeps through capillaries into surrounding tissue)
  • most of this interstitial fluid returns to blood through venule walls
    > remainder enters the lymphatic vessels
65
Q

How is lymph returned to blood circulation?

A
  • thoracic duct > collects lymph from whole body except right arm/ right side of head > empties into left subclavian vein
  • lymph from right arm/ right side of head collected > right lymphatic duct > drains into right subclavian vein
66
Q

What are the divisions of the lymph nodes?

A
  • Cortex > B cells/ macrophages/ follicular DCs
  • Paracortex > T cells/ DCs
  • Medulla > sparsely populated lymphoid cells/ plasma cells
67
Q

How does antigen enter lymph nodes?

A
  • antigen enters cortex via afferent lymphatic vessels
    > either in particulate from/ presented on surface of migrating APCs
  • particulate antigen can be presented on surface of resident DCs in paracortex
68
Q

How do T cells enter lymph nodes?

A
  • T cells enter cortex through HEVs (high endothelial venules)
  • browse MHC-peptide complexes on DCs in the paracortex
69
Q

What happens to T cells in lymph nodes?

A
  • T cells browse MHC-peptide complexes on DCs in the paracortex
  • if bind MHC-peptide complex > proliferate/ differentiate > effector cells
  • if do not bind MHC-peptide complex > exit lymph node via efferent lymphatics in medulla (not via blood)
70
Q

What allows T cells to browse APC surfaces in lymph nodes?

A
  • APCs wrap themselves around long processes of FRCs
    > gives T cells ample opportunity to browse MHC-peptide complexes
  • fibroblastic reticular cells (FRCs) in paracortex guide T cell movements
71
Q

What happens to B cells in lymph nodes?

A
  • like T cells enter via HEVs (high endothelial venules)
  • migrate to follicles > bind/ process antigen > present on surface > partially activated
  • moves to paracortex > binds to Th cell that recognizes its antigen-MHC surface > becomes fully activated
72
Q

What regulates the activation of B cells in lymph nodes?

A
  • FDCs (follicular dendritic cells) in follicles
    > FDCs are not pAPCs/ do not activate naive T cells
73
Q

What are the different types of B cell follicles?

A
  • Primary follicle > follicle without a germinal center
  • Secondary follicle > follicle that develops a germinal center
74
Q

Where does antigen affinity of B cells increase?

A
  • affinity maturation in germinal centers of follicles
    > somatic hypermutation of BCR genes of a proliferating B cell clone
  • cells with highest affinity receptors survive/ differentiate > plasma cells
75
Q

Where are plasma cells located?

A
  • some stay in medulla (lymph node)
  • some exit LN via efferent lymphatics > bone marrow
  • whether in LN/ bone marrow > release antibodies > bloodstream
76
Q

What is the main role of the spleen?

A
  • filters blood > first line of defence against blood-borne antigens
77
Q

What are the 2 main compartments of the spleen?

A
  • Red pulp > where old/ defective RBCs are removed
  • White pulp > where immune response initiated
78
Q

How do antigens enter spleen?

A
  • blood-borne antigens enter spleen through splenic artery
    > spleen is not supplied by lymphatic vessels
  • antigens interact with cells at marginal zone
    > antigen trapped/ processed by DCs > travel to PALS

PABI 6100 Immunobiology (6 decks)

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