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Immunology > Innate immunity > Flashcards

Innate immunity Flashcards

1
Q

Innate immunity mechanism

A
  • defensive function is early after infection
  • recognizing molecular structures, products of damaged and dead host cells and eliminate them
  • initiate tissue repair
  • induce Inflammation
  • stimulate adaptive responses
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2
Q

Structrual components that enable the immune System to recognize the invading pathogen /microbe

A
  • pathogen-associated molecular Patterns (PAMPs)
  • microbe-associated molecular Patterns (MAMPs)
  • Damage-associated molecular Patterns (DAMPs)
  • pattern recognition receptors (PRR)
  • toll-like receptors
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3
Q

PAMPs and MAMPs

A
  • microbial substances that stimulate innate immunity

- differenc tclasses of microbes express different PAMPS and MAMPs

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4
Q

DAMPs

A
  • endogenous molecules that are released from damaged and dying cells
  • may be produced as a result of cell Damage caused by infections, chemical Toxins, burns, tauma….
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5
Q

PRR (pattern recognition receptors)

A
  • cellular receptors for pathogens and Damage associated meolecules
  • -> recognize PAMPs, MAMPs, DAMPs
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6
Q

Types of PRRs

A

Toll like receptors: on Plasma membranes of dendritic cells and phagocytes and recognizes various microbiel molecules

NOD like receptor: in cytoplasm of phagocytes and recognized bacterial cell wall peptidoglycans

RIG like receptors: in cytoplasm of phagycytes and recognizes viral RNA

C type lectin like receptors: on Plasma membrane of phagocytes and recognized microbial Surface carbohydrates

Scavenger receptors: in plama membrane of phagocytes and recognizes microbial diacylglycerides

N-Formyl met-leu-phe receptors: in Plasma membrane of phagycytes and recognizes Peptides containing N Formyl……

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7
Q

Epithelial barrier

A
  • Skin and mucosa of GI, respiratory and genitourinary tracts
  • intact epithelium is physical barrier
  • epitheliocytes produce antimicrobial substances (antibiotics, defensins, calthelicidins)
  • kill microbes and infected cells by intraepithelial lymphocytes
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8
Q

Sequential steps of phagocytosis

A
  • recruitment of cells to the sites of infection
  • recognition of microbes and activation
  • Ingestion of microbes
  • destruction of ingested microbes
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9
Q

Neutrophils

A
  • mediate the earliest phases of inflammatory reactions

- circulate in blood for inly about 6 h and may migrate to sites of infection after a few Hours after entry of microbes

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10
Q

NETosis

A

neutrophul extracellular traps (NET) –> Network of extracellular fibers

  • neutrophils form Chromatin fibers
  • disarm pahtogens with antimicrobial proteins that have a high Affinity for DNA
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11
Q

Monocytes / Macrophages

A
  • when monocytes enter tissues –> mature macrophages
  • respond more slowly than neutrophils but for longer tome
  • typical for chronic Inflammation
  • repair damaged tissue
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12
Q

Recruitment of phagocytes

A
  • chemokines and adhesion molecules –> key roles
  • when cytokines are produces at site of infection –> enter Endothelium
  • adhesion molecules on phagocytes –> cytokines Change structure of adhesion molecules

Rolling: selectins and selectin ligans and Integrins and integrin ligans bind and phagocyte moves to the place of origin if tge chemokines

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13
Q

Microbiocidal molecules in phagolysosomes

A

lysosomal Enzyme
ROS
nitric oxide

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14
Q

Opsonization and opsonins

A

Process of attaching opsonins to micobial surfaces to target the microbes for phagocytosis

opsonins: macromolecules arraching to Surface of microbes

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15
Q

When neutrophils and macrophages are activated too strongly

A
  • -> can injure Healthy tissue by release of lysosomal Enzymes, ROS and nitric oxide
  • -> they cannot distinguish between self tissues and microbes
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16
Q

Chronic granuloma disease

A

caused by deficeincy of one of the components of phagocyte oxidase
–> comprosmises capacity of neutrophils to kill certain species of Gram positive bacteria

17
Q

Innate lymphoid cells

A

derived from common lymphoid progenitos and functionally similar to T cells
–> lack TCR!

18
Q

NK cells

A
  • mononuclear lymphocytes distinct from T and B cells
  • most recognize class I Major histocompatability complex (MHC) molecules
  • inhibitory receptors recognize MHC and therefore do not kill normal host cells
  • they kill cells in whihc class I MHC Expression is reduced
19
Q

Killing mechanism of NK cells

A
  • release of granules with perforin and granzymes
  • activation of Fas-FasL pathway
  • induction of apoptosis and DNA Fragmentation

function: killing of infected cells, release of IFN-g, activation of macrophages

20
Q

Complement system

A

several Plasma proteins that work together:

  • to opsonize microbes
  • to promote the recruitment of phagocytes
  • to directly kill the microbes

activation involves proteolytic cascades:
- inactive Enzyme (Zymogen) is altered to become active Protease that cleaves and thereby induces the proteolytic activity of next complement protein

21
Q

Three pathways of complement activation

A
  • classical pathway (by antibodies=
  • alternative pathway
  • lectin pathway
22
Q

Other soluble Plasma proteins

A
  • pentraxins: recognize microbial strctures
  • acute-phase reactants
  • Short pentraxins: CRP, Serum amyloid P
23
Q

Inflammation

A

Major way by which immune System deals with infections and tissue injury

accumulation of leukocytes, Plasma proteins, fluid derived from blood at site of infection…

24
Q

Local Actions of cytokines in inflammation

A

Endothelial cells: TNF and IL-1 –> increased permeability and secretion of chemokines and IL-1?

Leukocytes: TNF and IL-1 activate it and then it secretese IL1, IL6 and chemokines

25
Q

Systemic Actions of cytokines ininflammation

A

PROTECTIVE
Brain: TNF, IL1, Il6 –> Fever
Liver: IL1, IL6 –> acute Phase proteins
Bone marrow: TNF, IL1, IL6 –> leukocyte production

PATHOLOGICAL
Heart: TNF –> low Output
Endothelial cells: TNF –> Thrombus, increased permeability
Multiple tissues: TNF –> Insulin resistance

26
Q

Inflammosome

A

multiprotein compley includinf NOD like pattern recognition receptor 3 and caspase I

  • proteolytic activity generates acitve form of IL1
  • located in cytosol of phagocytes, dendritic cells and others
  • implicated in pathogenesis of many inflammatory diseases
  • Formation induced by PAMPs, DAMPs,insoluble crystals
27
Q

Proinflammatory cytokines

A

soluble proteins secretes by activated macrophages and others

  • TNF
  • IL1, IL6
  • IFN (Interferons=

autocrine Action: cytokine secreted by cell activates the same cells
paracrine Action: cytoine activates the neighboring cell

28
Q

Septic shock

A

comlication of severe bacterial Sepsis including vascular collapse, disseminated intravascular coagulation and metabolic disturbances

–> caused by LPS released by Gram negative bacter and massive production of TNF

29
Q

Components of innate immunity that stimulate adaptive immunity

A
  • APCs induce T cell activation and Differentiation
  • complement Fragments in alternative pathway provide second Signals for B cell activation
  • adjuvants: substances that Need to be adminisetered together with protein Antigens (vaccines) to elicit maximal T cell dependent immune responses
30
Q

Negative Feedback mechmanisms that regulate innate immune respones

A
  • Limit potential Damage to tissues
  • IL10: produced by macrophages and dendritic cells
  • -> inhibits their activation
  • -> blocks the activating Signals

Immunology (7 decks)

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