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Human Body_TP > Immune System Physiology: Innate System > Flashcards

Immune System Physiology: Innate System Flashcards

1
Q

immunity: a tradition predating history

A

-innate immune system is highly conserved
-around for years and has evolved over time
Ex. drosophila, starfish, frogs, chickens, zebrafish —> all have immune systems similar to humans

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2
Q

what is the biggest challenge of innate immunity?

A

recognizing major classes of organisms that cause problems

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3
Q

what are the four categories of organisms that are threats to the immune system?

A
  1. viruses
  2. intracellular and extracellular bacteria
  3. fungi
  4. parasites
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4
Q

what is the goal of innate immunity?

A

-recognize anything that falls within the four broad classes
-want to swiftly and efficiently ID potential health threats and
1. slow or halt their invasion
2. alert adaptive immune system
3. minimize damage to the organism

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5
Q

why are the majority of potential threats no threat at all?

A

the innate immune system is so effective

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6
Q

innate immune system is very fast-acting

A

causes inflammation, complement activation, phagocytosis, and destruction of pathogens within minutes and can last for days

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7
Q

what are the three main jobs of the innate immune system?

A

avoidance, resistance, and tolerance

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8
Q

physical and chemical barriers (avoidance)

A

-epithelial barriers
-mucus
-enzymes
-pH
-commensal microflora

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9
Q

professional profilers (resistance)

A

-humoral components
-cellular components

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10
Q

pathogen pathway

A

anatomic barriers (skin, oral mucosa, respiratory epithelium, intestine) —> complement/antimicrobial proteins (C3, defensins, Regllly) —> innate immune cells (macrophages, granulocytes, natural killer cells) —> adaptive immunity (B cells/antibodies, T cells)

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11
Q

prevention of damage (tolerance)

A

tolerate area to prevent extensive damage

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12
Q

cellular components of innate immunity

A

macrophages, dendritic cells, neutrophils, eosinophils, basophils, mast cells, and natural killers (NK) cells

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13
Q

macrophages

A

-huge component of the innate immune system- very specialized
-arise during embryonic development
-added by monocytes circulating blood
-have long lives like microglia living for decades
-major phagocytotic cell

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14
Q

what are the functions of macrophages?

A

-engulf pathogens and destroy them
-help orchestrate the innate immune system by putting out cytokines and letting other cells know about an infection
-when an infection has spread, they stick around and transition to repair- they help with tissue repair

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15
Q

monocytes —> macrophages

A

monocytes are the precursors to macrophages and they both have phagocytotic capabilities

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16
Q

what happens if you have too many microphages sticking around to repair?

A

could cause fibrosis in the liver or other issues near the site of infection

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17
Q

dendritic cells

A

-capability to phagocytose but actually do macropinocytosis, which is the drinking of the area around them with long dendrites that help with surveillance
-also in tissues like macrophages
-leave the site of infection and exit to the lymph node to get T cells

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18
Q

what do dendritic cells do?

A

survey for infection —> find it —> report it to specialized cells

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19
Q

what are three different granulocytes?

A

neutrophils, eosinophils, and basophils

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20
Q

neutrophils

A

-help phagocytose pathogens and spill innards to catch pathogens —> can cause tissue destruction
-leave bone marrow at night and in the morning they are very active then die

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21
Q

eosinophils and basophils

A

granulocytes released to kill pathogens but primarily focus on parasites and allergic responses

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22
Q

mast cells

A

respond to allergies by releasing histamines

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23
Q

natural killer (NK) cells

A

-bridge from innate to adaptive immune systems
-respond with specificity but not as much as adaptive
-release granules to pathogens

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24
Q

platelets

A

part of the circulating innate immunity system

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25
Q

innate-like lymphocytes

A

these are located within the tissue and they are cells that look like lymphocytes but innate functions since not that specific
Ex. ILCs in the gut, NK T cells, beta-alpha T cells (skin defense), and B-1 B cells (mouth for cavity defense)

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26
Q

circulating innate immunity

A

granulocytes (neutrophils, basophils, eosinophils), mast cells, monocytes, NK cells, platelets

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27
Q

tissue/cavity innate immunity

A

macrophages, dendritic cells, innate-like lymphocytes

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28
Q

macrophages + dendritic cells

A

-macrophages and dendritic cells- antigen-presenting cells of innate immunity- link between innate and adaptive immune systems
-present antigens to T and B cells to induce adaptive response
-without them there would be no way to tell adaptive system what to respond to

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29
Q

what induces an adaptive response?

A

interaction between macrophages, T cells, B cells, and dendritic cells

30
Q

how does the innate immune system ID potential threats?

A

pattern recognition receptors (PRRs)

31
Q

PRRs

A

-allow for innate immune system to respond w/in hour
-invariant in genome and don’t require recombination to form a specific receptor
-expressed rapidly and upregulated rapidly in response to infection

32
Q

pathogen associated molecular patterns (PAMPs)

A

-structural patterns common in pathogens that allow PRRs to accurately ID patterns
-conserved on pathogens for PRRs to recognize

33
Q

PAMPs

A

-bacteria (gram positive or gram negative) like lipoteichoic acid LTA, peptidoglycan PGN, lipoproteins, DNA, flagellin, and lipopolyssacharide LPS
-viruses
-parasites
-yeast
-there are specific building blocks in these pathogens that without them they won’t survive and the immune system evolves to respond to these pathogens

34
Q

what are some defense mechanisms of the PAMPs?

A

-viruses have coat proteins that prevent the immune system from seeing them
-parasites have GPI anchors
-bacteria are able to go intercellular and begin replication inside Ex. salmonella
-yeast have zymosan (beta-glucan)

35
Q

what are the two types of PRRs?

A

humoral and cellular

36
Q

humoral PRR

A

-made by the liver and circulates in the blood
-CI complex of complement
-mannose-binding lectin
-C reactive protein
-surfactant proteins like A and D in the lung that create poor environment for bacteria
Ex. complement sets off chain reaction —> creates pore in lipid bilayer of bacteria

37
Q

what does mannose-binding lectin do?

A

binds to the mannose in the cell surface of bacteria and yeasts and activates the complement system

38
Q

cellular PRRs

A

extracellular and intracellular

39
Q

extracellular PRRs

A

-extracellular membrane bound
-phagocytic receptors: recognize mannose-binding lectin, complement-bound cells, scavenger receptors
-signalling receptors: toll-like receptors (TLRs) 1, 2, 4, 5, 6

40
Q

intracellular PRRs

A

-membrane bound: TLRs 3, 7, 8, 9
-cystolic in the cytosol of the cell like NOD1 and 2, inflammasomes

41
Q

extracellular TLRs

A

-extracellular proteins that recognize something that lives outside the cell
-TLR1:TLR2 and TLR2:TLR6 are heterodimers on the surface of cells —> recognize different ligands associated with bacteria or yeast
-TLR4 recognizes LPS on bacteria

42
Q

intracellular, membrane-bound TLRs

A

-primarily focused on viruses since they only survive inside cells
-TLR3- dsRNA
-TLR7- ssRNA
-TLR8- G-rich oligonucleotides
-TLR9- unmethylated CpG DNA

43
Q

TLRs

A

best known PRRs

44
Q

downstream of the TLRs

A

Ex. TLR4
-LPS binds to it —> cascade of MyD88 —> interferon kappa (IkBa) —> pro-inflammatory cytokines
-TLR4 induces MyD88 cascade which leads to NfKB and also an interferon cascade —> IRF3 and interferon production

45
Q

what occurs when a PAMP binds to a PRR?

A
  1. destruction of PAMP’s source
  2. recruitment of other cells
  3. priming of PRR-bearing cells
46
Q

what are ways of destroying the PAMP’s source?

A

phagocytosis, cytotoxic killing, secretion type I IFNs: interferon alpha and beta, and inducing “climate change”

47
Q

phagocytosis

A

-through mannose-binding lectin bind to the outside of the pathogen or cell-to-cell interaction
-macrophage sees bacteria and phagocytoses it
-done by neutrophils and macrophages
-irreversible oxidative destruction

48
Q

how does a macrophage kill a pathogen?

A

bacteria that binds to a complement receptor —> bacteria is coated in complement —> brought in by phagosome —> merges with lysosome with low pH that wllows for oxidative pathways to destroy the pathogen

49
Q

how do neutrophils kill a pathogen?

A

bacteria gets into lysosome —> enters into phago lysosome —> gets destroyed by oxidative destructive pathways

50
Q

cytotoxic killing

A

-through membrane attack complex
-series of different C proteins that follow a specific chain of command
-end result of complement is formation of C9 pore —> leads to destruction of pathogen where all the sodium exits and it dies

51
Q

NK cells

A

-kill with perforin
-a lot of positive and negative receptors- positive more than negative then you have degranulation and the same effect with the membrane and Na gradient shifting
-granzyme and granulysin —> apoptosis

52
Q

secretion of Type I IFNs: interferon alpha and beta

A

-very potent cytokines and they bind to interferon receptors and lead down pathway of induction
-tell cells that see PAMP to turn on restriction factors and the nearby cells to turn them on —> inhibits replication of viruses and creates a silo of replication

53
Q

inducing “climate change”

A

-fevers induce global climate change
-macrophages secrete IL-1B, IL-6, TNFalpha —> acts on different organs for specific functions
-liver- has acute phase protein synthesis, which activates complement opsonization
-bone marrow endothelium- releases neutrophils which lead to phagocytosis
-hypothalamus- increase the body’s temperature
-fat and muscle- increase the body’s energy and and cell response
-dendritic cells- get help from the lymph nodes

54
Q

mast cells, monocytes, and platelets

A

-not only do the dendritic cells leave but others involved
-neutrophils and monocytes in the blood normally just circulate but sometimes they attach to vessels to draw away

55
Q

vasoactive peptides

A

-production of vasoactive peptides like histamines and serotonin and cytokines from monocyte, mast cells, and platelets
-takes blood vessel and makes it leaky for cell to leave near infection

56
Q

TNFalpha

A

-induces integrins and selectins, which increases the permeability
-monocytes bind to these on the endothelium and as the amount increases in a row, it slows down the cells

57
Q

what are involved in recruitment of other cells?

A

-vasoactive peptides and cytokines, activating cytokines and chemokines, and the end result: rolling and diapedesis
-essentially the role is to get cells to exit the blood vessels and follow the bread crumbs to infection
-CCL2 engages monocytes, CCL8 engages neutrophils and T cells

58
Q

chemokines

A
  1. monocytes, macrophages, and dendritic cells —> CCL2 —> monocytes
  2. macrophages and endothelial cells —> CXCL8 AKA IL-8: neutrophils and T cells
59
Q

cytokines: Signal 3 —> Th1 vs Th2

A
  1. platelets —> RANTES —> monocytes
  2. macrophages —> IL-12 —> NK cells
  3. macrophages —> IL-1beta and IL-6 —> lymphocytes
60
Q

Th1 + Th2

A

types of helper cells that differ in their roles in the immune system and the cytokines they release

61
Q

Th1 cells

A

produce cytokines such as IL-2 and IFN-γ

62
Q

chemokines role in recruiting other cells

A

-need chemokines and cytokines to be produced simultaneously and they filter out to blood
-monoctyes or neutrophils recognize a chemokine with a receptor on its surface and a lot of CCL2 will draw them in that direction
-CXCL8 is the same idea but with neutrophils and T cells and pulls them from blood to site of infection

63
Q

cytokines role in recruiting other cells

A

drive platelets and macrophages to a particular pathway

64
Q

rolling and diapedesis

A

rolling adhesion with the CXCL8R —> tight binding —> diapedesis (passage of blood cells through the capillaries) —> migration to site of infection

65
Q

priming of PRR-bearing cell

A

-upregulation of two important proteins: MHC Class II or MHC Class I
-MHC II and I present peptides to adaptive system
-MHC II: macrophages and dendritic cells
-MHC I: all cells, including neurons, except for RBCs
-must present the peptide in context

66
Q

MHC Class II

A

take invading pathogen —> put it on peptide holding protein —> show CD4+ or CD8+ to get them to generate a response

67
Q

MHC Class I

A

CD8 will kill the pathogen

68
Q

what is needed to activate CD4+?

A

upregulation of MHC I/II must include a co-stimulatory molecule to activate CD4+ —> cannot activate T cell through one signal

69
Q

where does activation of CD4+ or CD8+ occur?

A

-dendritic cells travel to the lymph node near site of infection (like in the armpit, arms and legs, neck, breasts) and present to T cells that are circulating in the lymphatic vessels
-naive T cells will bind to the antigen and once the infection has happened, there is a ramp-up of T cells

70
Q

what is involved in the priming of PRR-bearing cells?

A

upregulation of MHC II or MHC I, induction of co-stimulatory molecules, and migration to lymph node

71
Q

summary of innate immune system

A

-innate immune system has PRRs recognize PAMPs
-slow/halt expansion through the humoral/cellular components
-destroy PAMPs and recruit other cells

72
Q

example of cut

A

-pathogen in cut —> infection —> recruit cells to kill it and it fails —> recruit macrophages and dendritic cells and they fail —> adaptive immune system comes in
-get through failure points and adaptive system kicks in

Human Body_TP (16 decks)

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