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Immunology Med School wk 1 > Innate Immunity Activation Lecture > Flashcards

Innate Immunity Activation Lecture Flashcards

1
Q

Innate defensive components:

Anatomic & physical barriers

A

effectors: skin, mucous membranes, temperature, acidic pH, lactic acid, chemical mediators

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2
Q

Innate defensive components:

Immune cells

A

effectors Granulocytes: phagocytosis, release of mediators. macrophages: phagocytosis, release of mediators, Ag presentation

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3
Q

Innate defensive components:

Inflammatory mediators

A

effectors: complement, cytokines, lysozyme, acute-phase proteins, leukotrienes and prostaglandins

function: lysis of pathogens, activation of immune cells
bacterial cells wall destruction
mediation of reponse
vasodilation, vascular perm.

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4
Q

Skin: mechanical/Chemical/Microbiological roles

A

M: flow of fluid, perspiration, sloughing off skin
C: Sebum (contains fatty acids, lactic acid, lysozyme)
M: normal flora of the skin

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5
Q

Gastrointestinal tract: mechanical/Chemical/Microbiological roles

A

M: Flow of fluid, mucus, food and saliva
C: acidity, protease enzymes
M: normal flora of the GI

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6
Q

Resp. Tract: mech/chem/micrbio roles

A

M: flow of fluid, mucus, cilia by air flow
C: lysozyme in nasal secretions
M: normal flora of rest t.

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7
Q

Urogenital tract

A

M: flow of fluid, urine, mucus, sperm
C: acidity in vaginal secretions/sperm
M: normal flora

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8
Q

Eyes

A

M: flow of fluid
C: lysozyme in tears
M: normal flora of the eyes

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9
Q

“natural immunity” is associated with which aspect of the immune system?

A

innate

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10
Q

What does “PRP” represent for innate immunity?

A

Phagocytosis
Recruitment
Presentation

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11
Q

Neutrophils: high lighted points

A

1) first cells to arrive at site of tissue damage

2) activation leads to respiratory burst and release of granules to control bacterial growth

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12
Q

Macrophages: high lighted points

A

Engulf organisms
Release inflammatory mediators

THEY DO NOT LEAVE THE TISSUES

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13
Q

Eosinophils: high lighted points

A

contain cationic granules (basic protein, peroxidases, antimicrobial proteins)

fight HELMINTHES and multicellular parasites

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14
Q

NK cells: high lighted points

A

large, granular lymphocytes that kill infected host cells by cytolytic mediator perforin

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15
Q

Neutrophils and Monocytes

Where they arive, how they get to sites of inflammation/infection

A

they arise in bone marrow

they are ready to be activated, and do not require activation

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16
Q

How do neuts and monocytes physically access tissues where they are recruited?

A

they are recruited through post-capillary venules EXCEPT for parenchymal tissues like lungs, liver, kidneys
where all WBCs enter through capillaries

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17
Q

name the 3 functions of myeloid leukocytes

A

elimination of infectious pathogens
clear dead tissues
repair the damage

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18
Q

“how neutrophils come into the tissues”

inflammation activated endothelial cells express which selectins? and in response to what?

A

E and P selectin

P selectin arises in response to histamine
E selectin arises in response to IL-1 and TNF from Macrophages

both P and E are used by monocytes and neutrophils

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19
Q

“how neutrophils come into the tissues”

Chemotaxis the 4 general steps

A

1) Neutrophils “slow down and roll” along endothelium
i. selectin-selectin co receptor interactions
2) tight binding
i. integrins (on leukocytes) and integrin ligands (on
endothelia)
3) Diapedesis
i. transmigration through endothelium
4) Chemoattractant controls migration (IL-8 controls neutrophil migration to inflammatory sites)

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20
Q

LFA-1

What is it?
What is its receptor?

A

neutrophil integrin (low affinity integrin-1)

its affinity for its ligand increases as chemokine IL-8 binds to chemoattractant receptor on cell

ICAM-I is LFA-1’s receptor

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21
Q

ICAM-1

A

neutrophil integrin LFA-1’s endothelia receptor

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22
Q

Transmigration of Leukocytes “big” picture steps

A

1) capture: mediated by selectin
2) rolling: mediated by selectin
3) activation: IL-8 (neutrophils), MCP-1 (monocytes)
4) arrest: VCAM-1 (Baso/Eosino/Mono), ICAM-1 (neutro)
5) firm adhesion VCAM-1, ICAM-!
6) transmigration

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23
Q

IL-8

A

mast cell released chemoattractant for neutrophils

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24
Q

ICAM-1

A

endothelial neutrophil integrin receptor (LFA-1)

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25
Q

LFA-1

A

neutrophil integrin

26
Q

VCAM-1

A

integrin receptor for lymphocytes, baso/eosino/monocytes

27
Q

MCP-1

A

monocyte chemoattractant, secreted by macrophages apparently

28
Q

neutrophil/monocyte capture is regulated by

A

selectins

neuto

29
Q

neutrophil rolling is regulated by

A

selectins

30
Q

neutrophil activation is regulated by

A

chemokines IL-8 for neuts and MCP-1 for monocytes

31
Q

neutrophil/monocyte arrest

A

achieved by integrin/receptor interactions

integrins are on the neuts/monos, receptors like ICAM-1 and VCAM-1 are on the endothelia

32
Q

Cathepsin G

A

released by neutrophils

cationic protein, a serine protease that digests collagen and proteoglycans

33
Q

Lysozyme

A

released by neutrophils

splits mucopeptide in bacterial cell wall

34
Q

Lactoferrin

A

released by neutrophils

bacteriostatic protein
complexs with iron

35
Q

Defensins

A

released by neutrophils

cationic (rich in Arg): antibiotic peptides
- inserts into microbial membranes –> destabilizes ion channels

36
Q

what pathogens are defensins good against?

A

gram +/- pathogens, fungi, enveloped viruses

37
Q

BPI

A

bacterial permeability increasing protein

released by neutrophils

38
Q

Transmigration of MONOCYTES (not neutrophils)

A

rolling, adhesion, and diapedesis (steps 1-3) are the same for monocytes as for neuts

chemoattractants for monocytes are
Macrophage inflammatory protein-1alpha/beta (MIPs)
Monocyte chemoattractant protein-1 (MCPs)

39
Q

what do monocytes do after entering tissues?

A

they mature into tissue macrophages

40
Q

M1

what, what do they do

A

classical macs: activated by IFN-gamma to destroy pathogens

secrete cytokines IL-1, 12, 23 (inflammation)
Possess intracellular microbicidal actions (ROS, NO etc)

41
Q

M2

A

Anti-inflammatory macs

secrete IL-10 and TGE-beta to prevent the effects of IL-1 and IL-12 and IL-23 chemokines from initiating inflammation

prolines, polyamines, TGF-beta for wound repair, fibrosis)

42
Q

what chemokines are responsible for inflammation in M1s? how are they suppressed?

A

IL-1, 12, and 23

by IL-10 from M2s

43
Q

TGF-beta

A

M2

suppresses the effects of M1’s cytokine output (IL-1, 12, 23) and initiated wound repair by attracting fibroblasts

44
Q

what cytokines induce M2?

A

IL-4 and IL-13

45
Q

what induces M1?

A

TLRs and IFN-gamma

46
Q

PRR triggered responses in neutrophils and MO

what is a substrate present in prokaryotes that aren’t in eukaryotes

A

fMet

N-formylmethionyl peptide

47
Q

who recognizes fMet and what do they do

A

polymorphonuclear cells, they initiated phagocytosis

48
Q

what is the functional outcome of fMet recognition

A

cytokins/chemokines signal to the endothelia for recruitment, then migration

49
Q

Mannose receptor results in

A

both phagocytosis and cytokine production

50
Q

Ligands/functions/PRRs

C type lectin (protein family)

A

mannose receptor on mac, phag

51
Q

Scavenger receptors: name two and their ligands

A

SR-AI, SR AII

bind to anionic polymers

macs, phag

52
Q

TLRs (again) 5 goes to…..

A

bacterial flaggela

53
Q

for whom are PRRs the most important? neutrophils or macs?

A

Macs

54
Q

NK cells: direct and indirect involvement

A

directly kill after recognition, indirectly kill by activating macs with IFN-gamma

55
Q

what activates NK cells?

A

IL-12

56
Q

NK cells: how they find their targets

A

two receptors, activating and inhibitory receptors

57
Q

Inhibitory receptor on NK cells: how

A

inhibitory receptor is composed of two signals = normal expression of MHC 1 + “activating ligand for NK cell”

if there’s a change in MHC I, the activation signal is left to activate the NK cell

58
Q

ADCC

A

antibody dependent cellular cytotoxicity

59
Q

Healthy cell activating receptors on NK cells

reduce this fucker to its simplest explanation

A

recognize ligands on target cells which activate the protein tyrosine kinase (PTK)

PTK is inhibited by inhibitory receptors that recognie class MHC molecules and activate protein tyrosine phosphatase (PTP)

the inhibitory signals cause PTP to DE-phosphorylate PTK, which prevents PTV from sending the activation signal from its extracellular ligand

60
Q

PTP and PTK

A

PTP prevents PTK from sending a signal inside natural killer cells

61
Q

PTK

A

sends activating signals inside the cell

62
Q

what happens in virus infected cells?

A

the inhibitory signal sent by MHC isn’t send, and the NK is activated

Immunology Med School wk 1 (36 decks)

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