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Immunology > Lecture 2- Innate Immune System > Flashcards

Lecture 2- Innate Immune System Flashcards

1
Q

PAMP-Pathogen Associated Molecular Patterns

A

Motifs that are entirely unique to non-self microbes, something immune system can recognize due to pattern difference

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2
Q

PRR-Pattern Recognition Receptor

A

Cellular Receptors that recognize PAMPs

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3
Q

Cytokine

A

Soluble molecules that modulate immune response

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4
Q

Chemokine

A

Soluble molecules that set up a gradient of chemoattractants to the site of infection

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5
Q

Type I IFN- Type I Interferon

A
  • Cytokine made by innate immune response PAMP sensing that modulate immune response to fight.
  • virus infection recognized by PRR -> cell makes IFN -> IFN Autocrine Effect: -cell shuts down normal functions/goes into antiviral state Paracrine Effect: Other cells put up their defenses
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6
Q

TLR- Toll Like Receptors

A

PRRs that primarily recognize PAMPs- signal through MyD88 and TRIF (TLR3)

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7
Q

IRF-Interferon Regulatory Factor

A

Transcription factors that control interferon production and some interferon responses

  • Type I and III are innate, type II is adaptive
  • All nucleated cells make and respond to Type I IFN
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8
Q

Levels of Innate Immunity

A

Barriers: physical, chemical, microbial
Molecular: Complement, Antimicrobial peptides, Antimicrobial Enzymes
Cellular: Natural Killer Cell,
Dendtritic cell, Macrophages/Monocytes, Neutrophil

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9
Q

Physical Barriers

A

Physically block pathogen from entering host,
Strong barriers: skin, hair, nails
Vulnerable barriers: mucosal membranes

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10
Q

Mucosal Surface Barriers

A

Physical and Chemical: cilia move mucous around, up and out, slows down microbes, helps body expectorate microbes
Microbial: Good flora provide resource competition for pathogenic flora, can produce toxins that inhibit other microbes

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11
Q

Molecular Defenses

A
  1. Antimicrobial Peptides
  2. Complement
  3. Antimicrobial Enzymes
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12
Q

Antimicrobial Peptides

A
  • Defensins, Cathelicidins, Histatins
  • Activated by proteolysis (cut off regulatory piece, leaves active piece)
  • Amphipathic (hydrophillic and hydrophobic parts, helps insert into membrane to make pores)
  • Form pores in membranes
  • Made by epithelial cells
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13
Q

Complement

A

-Enzymatic cascade that leads to inflammation, neutrophil recruitment and pore formation in membranes (can’t maintain membrane integrity=death)

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14
Q

Antimicrobial Enzymes

A
  • Lysozyme: in tears, saliva, phagocytes, breaks peptidoglycan (outer cell layer in bacteria), helps other molecular defenses make pores
  • Phospholipase A : enters bacterial cell wall and hydrolyzes phospholipids, breaks down cell wall
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15
Q

Complement Pathways

A

Alternative: First pathway activated in body(innate) Involves interaction w surface of membrane, self-cells have off signals to end pathway
Classical: Part of adaptive response, requires prior antibody-antigen reaction
Lectin: Dependent on binding of lectin to surface mannose of pathogen, recruits proteins for enzymatic cleavage

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16
Q

Rest of Complement Pathway

A
  • all complement proteins referred to as C#*
  • All 3 pathways converge at C3 convertase
  • C3 convertase -> C5 convertase -> MAC (Membrane Attack Complex) formation: insertion of proteins into pathogen surface= loss of membrane integrity=cell lysis
17
Q

Antimicrobial Molecules

A
  • Work directly on microbes
  • Disrupt membranes
  • Inhibit metabolism
  • Physically slow or stop microbes (by binding to them) before they reach epithelial cell surface
  • Help immune cells identify (by binding to surface) and phagocytose microbes
18
Q

Innate Cellular Defenses

A
  • Neutrophil
  • Macrophages/monocytes
  • Natural Killer Cell
  • Dendritic Cells
19
Q

Phagocytes

A
  • Macrophages/monocytes and neutrophils
  • Engulf foreign bodies via phagocytosis -> phagosome fuses with lysosome -> pathogen death in phagolysosome
  • If pathogen doesn’t die via regular contact w lysosome, Macrophage receives activation signal from outside cells to use ROS and NO (bleach) and other lysosomal enzymes
20
Q

Neutrophils (PMN-polymorphonuclear leaukocyte)

A
  • Kamikaze cell -Short lived phagocyte -granules -most abundant WBC, make up pus, kill themselves to kill pathogen
  • Multi-lobe nucleus allows migration through tight spaces, no need for vasodilation to access infection
  • Change shape when activated to become amoeba like w pseudopods to hunt microbes
  • Use chemokine/cytokine greceptors to follow gradients to site of damage
  • Kill through phagocytosis, degranulation and Neutrophil Extracellular Traps (NETs)
21
Q

NETs- Neutrophil Extracellular Traps

A
  • Are condensed DNA thrown out of neutrophils to trap microbes due to negative charges
  • Signals phagocytosis and other immune cells
  • unique to neutrophils
22
Q

Macrophages

A
  • Garage collectors, clean up dead cells/debris -Use O2/NO to kill - Long lived phagocyte (lifetime)
  • Everyday function (no pathogen/inflammation): phagocytoses apotosis cells
  • Inflammation function: eliminates pathogens, antigen function
23
Q

Monocytes

A
  • Premature macrophage in blood
  • After chemokine signal, migrate out of blood and mature in the tissue into primarily macrophages
  • Can also become dendritic cells
24
Q

Natural Killer Cells (NK Cells)

A

-Hold me back, bro -Induced apoptosis for altered/absence of self cells (injured cells/tumors/infected cells)
-If NK cell receives more activating signals, then induces apoptosis in target, if receives more inhibitory signals, target survives
Degranulation: pokes holes in membrane to damage cell membrane integrity
Activates Death Receptors: sends receptors to damaged cell to induce apoptosis
ADCC ( Antibody Dependent Cellular Cytotoxicity): adaptive immune response, recognizes that call has antibody bound to it, binds to back end of antibody, induces apoptosis signal

25
Q

Dendritic Cells

A
  • Messenger -Resident in tissues -Bridge between innate and adaptive, recognizes pathogen and informs adaptive via lymphatic system
  • Takes up antigen -> lymphatic system -> lymph node -> presents antigent o T cell -> activate T cell =Adaptive immune response
26
Q

PRR action

A

PRR recognizes PAMP -> Adaptor molecules -> activation of NFkB and IRF transcription factors= NFkB activate pro-inflammatory genes/addaptive immune response, IRF activates Type I interferon genes-> antiviral state

27
Q

Extracellular PRRs

A

TLR-Toll-like Receptor: recognizes extracellular bacterial products
C type lectins: Recognize fungal polysaccharides

28
Q

Cystolic PRRs

A

NLR-Nod-like Receptor: recognizes cytosolic bacterial cell wall products
RLR-RIG-I-like Receptor: recognizes cytosolic viral RNA
CDS- Cytosolic DNA Sensors: recognize microbial DNA in cytosol, any DNA in cytosol is bad sign

29
Q

Endosomal PRRs

A

TLR- TLR-Toll-like Receptor: recognizes endosomal bacterial products

30
Q

Getting past innate immune system

A
  1. Containment by anatomic barrier (skin, mucous, cilia, low pH)
  2. Recognition by preformed non-specific and broadly specific effectors (neutrophils/macrophages)
  3. Recognition of PAMP’s activation of effector cells and inflammation (NFkB cascade, IFN)

Immunology (7 decks)

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