innate immune response Flashcards

1
Q

what is the overview of innate immunity?

A

pathogens cross over epithelial layers of skin, it binds to cells that activate phagocytosis, cytokines, chemokines, antimicrobial substances, killing by NK cells, and inflammation

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2
Q

the first line of defense against foreign pathogens…

A

physical barriers, such as the skin, mucosal tracts, secretory glands, cilia (hairlike protrusions), secretions, normal microbiota. they prevent physical attachment and/or entry of pathogens into the host

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3
Q

what does our microbiota do to protect us from invadign pathogens?

A

prime immune defenses, metabolic exclusion of pathogens, and uses antimicrobial antagonism

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4
Q

what is required for the development of GALT?

A

gut bacteria

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5
Q

why are secreted protective substances important at physical barriers?

A

they constitute the chemical barriers

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6
Q

protective substances include…

A

-antimicrobial proteins - enzymes, binding proteins
-antimicrobial peptides - alpha and beta defensins, cathelicidin, histatins
-acidic pH

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7
Q

what do chemical barriers aim at?

A

killing and inhibiting growth of pathogens by inhibiting DNA/RNA/protein synthesis, interfering with energy production, and forming pores and disrupting membranes

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8
Q

how do antimicrobial peptides target microbe membranes specifically?

A

electrostatic and hydrophobic interactions, as well as membrane disruption

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9
Q

what are the humoral factors in innate immunity?

A

complement system/opsonins

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10
Q

what immune functions are induced after PAMPs bind to PRRs?

A

production of cytokines/chemokines, production of antimicrobial peptides, expression of enzymes, oxidative burst, phagocytosis, antigen presentation, NETs ad NETosis (NK cells)

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11
Q

what are the TLR structural characteristics?

A

the exterior domain (outside the cell membrane) contains leucine-rich repeats, otherwise known as the PAMP-binding domain. the domain within the cell is the TIR domain

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12
Q

how does the structure of TLRs change upon PAMP binding?

A

TLRs dimerize, either becoming homo- or heterodimers. TLRs then interact with either MyD88 and TRIF adaptor molecules (all but TLR3 are MyD88 dependent)

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13
Q

what is the definition of phagocytosis?

A

cellular uptake of particulate materials by engulfment; a form of endocytosis

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14
Q

what are the receptors that trigger phagocytosis after PAMP recognition?

A

several PRRs such as CLRs, and scavenger receptors

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15
Q

what factor can enhance phagocytosis?

A

the binding of opsonins at the surface of microbes, referred to as opsonization. opsonization consists of complement proteins binding to bacterium, followed by the complex binding to the phagocytic cell.
opsonins are recognized by specific receptors found at the surface of immune cells

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16
Q

process of phagocytosis

A
  1. bacterium binds to PRRs on membrane evaginations called pseudopodia
    2.. bacterium is ingested, forming phagosome
  2. phagosome fuses with lysosome (phagolysosome)
  3. bacterium is killed and then digested by low pH-activated lysosomal enzymes
  4. Digestion products are released from the cell
17
Q

what are other killing mechanisms besides phagocytosis?

A
  1. enzymes - nitric oxide synthase (damages intracellular microbes)
  2. production of reactive oxygen species (ROS) via the phagosome NADPH oxidase enzyme complex
  3. production of reactive nitrogen species
  4. programmed cell death
  5. autophagy
  6. NETs (neutrophil extracellular traps)