L3- Innate Immunity Flashcards

1
Q

What is the innate system?

A

Non-adaptive host defense against pathogens

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2
Q

What are phagocytes?

A

Leukocytes that recognize, ingest, and kill invaders

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3
Q

Which cell si normally the first cell to encounter a pathogen?

A

MAcrophage

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4
Q

What is the most abundant WBC in circulation?

A

NEutrophils

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5
Q

Are macrophages or neutrophils uusally found in normal tissues?

A

macrophages

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6
Q

Which is longer lived, macrophages or neutrophils?

A

Macrophages

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7
Q

What is opsonization?

A

coating particles with molecules to enhance recognition by phagocytes

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8
Q

How can the adaptive and innate immune systems opsonize pathogens?

A

Adaptive: antibodies
Innate: complement

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9
Q

What are used by phagocytes to detect cells for phagocytosis?

A

PRRs to detect PAMPs on pathogens (TLRs, CLR, RLRs, NLRs,)

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10
Q

What are the 3 key events in inflammation?

A

Altered blood flow
Inc vascular permeability
Infiltration of white blood cells into affected area

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11
Q

What are the hallmarks of inflammation?

A

redness, swelling heat, pain

rubor, dolor, calor, tumor

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12
Q

In what order do the following arive to an affected area for inflammation?
macrophages
neutrophils
lymphocytes

A

neutrophils, then macrophages, then lymphocytes

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13
Q

What does the recognition of PAMPs/DAMPs lead to?

A

increased secretion of proinflammatory cytokines and antimicrobial proteins

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14
Q

What does the recognition of PAMPs/DAMPs lead to?

A

increased secretion of proinflammatory cytokines and antimicrobial proteins

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15
Q

What are some typical PAMPs?

A

Mannose containing structures
Lipids in lipopolysaccharids
Viral/Bacterial nucleic acids

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16
Q

What kind of pathogens do each PRRs act towards?

A

TLR: EC pathogen (bacterial)
CLR: sugar molecules not seen in host (fungi, bacterial)
NLR: conserve molecules of virus/bacteria in cells
RLR: recognize RNR molecules (viral)

17
Q

What is the most important cell in the immune ssytem? why?

A

DCs. They act as gateway from innate to adaptive response

18
Q

What kind of ligand does TLR-4 bind?

A

LPS

19
Q

What is the common path for pro-inflammatory activation in TLR activation?

A

NK-kB -> leads to activation of genes encoding proinflammatory cytokines

20
Q

What happens when the TLR is missing or incorrrectly activated?

A

Pathogen not sense and get uncontrolled replication of pathogen (no innate imunity )

21
Q

What do deficiencies in MyD88/IRAK4 lead to?

A

Pts are more prone to bacterial infections

More severe than defective TLR-4 persay since this is downstream of all TLRs -> make them all useless

22
Q

What are natural killer cells?

A

Small porption of lymphocytes that circulate in blood to destroy virally infected cells and cancer cells

23
Q

What are NKT cells?

A

Subset of T cells that are part of innate immun system. Has TCRs that target glycolipid antigens

24
Q

What do NKT cells do?

A

Provide immediate help for adaptive immune system via cytokines

25
Q

What do NKT cells recognize lipids in context of with their TCRs?

A

Recoginze in context of CD1 molecules

INNATE IMMUNE CELL

26
Q

How do NK cells kill their targets?

A

Direct killing of infected cells
OR
ADCC (Antibody dependent cytotoxicity): interface with adaptive via Fc receptors recognizing constant regions of immunoglobulins to destroy the virally infected cell coated with antibody)

27
Q

What are γδ lymphocytes?

A

REcognize small molecule phosphoantigens not seen in mammals. Similar to CD4+ T cells

28
Q

Where do you find γδ lymphocytes?

A

host-environmental interfaces (respiratory, GI submucosa)

29
Q

What makes up the primary lymphoid tissue?

A

Bone marrow and thymus

30
Q

What makes up the secondary lymphoid tissue?

A

Lymph nodes, spleen

31
Q

What are regional/specialized lymphoid tissue?

A

Submucosal lymphoid tissue (respiratory and GI)

32
Q

How is innate memory or trained memory established?

A

No gene rearrangements or somatic hypermutations. EPIGENETIC!

33
Q

Give a sequential overview of dealing with infection from innate to immune

A

Bacteria invade -> phagocytosis by Macrophage via PRRs -> increase chemokine & cytokine -> increase neutrophils and other innate cells to area -> DCs come and uptake bacteria -> mature DCs via PRRS -> go to lymph node –> present to T/Bcells -> increase T cell differentiation and production of antibodies -> leave lymph node to site of infection-> clear infection