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Immunology > cytokines, acute phase reactions, defensins > Flashcards

cytokines, acute phase reactions, defensins Flashcards

1
Q

what stimulates inflammation

A

activation of innate immune cells by pathogens

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2
Q

responses go inflammation

A

swelling, redness, heat, pain, loss of function

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3
Q

what happens when inflammation fails to give a resolution

A

leads to fibrosis, septic shock and chronic inflam

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4
Q

t and b cell pathogen detection

A

individual t and b cells are highly selective for a specific pathogen species
immune memory for a faster secondary response

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5
Q

innate immune cell pathogen detection

A

less selective than t and b, recognise broad classes of pathogens and not specific species, no immune memory, 1st line of defence
detect pathogens via pathogen associates molecular patten

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6
Q

PAMP

A

pathogen associates molecular pattern

molecules or structures that are specific more microbes and viruses not visible to host cells

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7
Q

PRR

A

pattern recognition receptor

invariant germline encoded receptors

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8
Q

where are PRRs expressed

A

on innate immune cells and in some t, b and endothelial cells

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9
Q

classes of PRRs

A

toll like, nod like, c type lectin, dna and rna

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10
Q

what are cytokines

A

small proteins that mediate cell-cell communication during immune reactions
can have multiple targets

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11
Q

where are cytokines produced

A

cells in the immune system

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12
Q

main action of cytokines

A

on the immune system, some circumstances they target non immune cells

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13
Q

how do cytokines stimulate cells

A

via cytokine receptors

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14
Q

difff classes of cytokines

A

chemokines, interleukins and TNF

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15
Q

what to cytokines recruit

A

immune cellss

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16
Q

what do classical cytokines modulate

A

immune cell function

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17
Q

what effect do chemokines have

A

homeostatic or immune effects on leukocyte migration

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18
Q

chemokine types

A

4 groups divided based on the position of cysteine residues that mediate the formation of disulphide bridges in their 3d conformation

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19
Q

what do macrophages secrete

A

inflammatory cytokines, IL-1beta, TNFalpha, IL-6, CXCL8, IL-12 - all leads to inflammation at site of infection

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20
Q

IL-1beta and TNFalpha from macrophages

A

induce blood vessels to become more permeable, enabling effector cells and fluid containing soluble effector molecules to enter infected tissues

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21
Q

IL-6 from macrophages

A

induces fat and muscle cells to metabolise , make heat and raise temp in infected tissue

22
Q

IL-12 from macrophages

A

recruits and activates NK cells that secrete cytokines that strengthen macrophages response to infections

23
Q

host defence peptides (HDP)

A

peptides that can initiate prokaryotic cells or viruses, produced by both proks and euks

24
Q

host defence peptides 3 main mechanisms of action

A

distribution of membrane integrity, bind precursors of cell wall formation to inhibit formation of bacterial cell wall and thus blocks bacterial replication, targets intracellular proteins to disrupt cell function

25
Q

mammalian host defence peptides

A

cathelicidin and defensins

26
Q

alpha defensins

A

restricted to certain mammalian species, mainly expressed in myeloid and paneth cells

27
Q

beta defensin

A

found in vertebrates and invertebrates immune and epithelial cells

28
Q

why are cytokines released

A

by macrophages in response to stimulation of pattern recognition receptors

29
Q

what doers release of cytokines require

A

de-novo transcription and translation of cytokine genes and is regulated at transcription, mRNA stability and mRNA translation

30
Q

what in cytokines allows their transport to the ER and subsequent secretion

A

their pro-sequence
(IL-1 and TNF are exceptions, IL-1b requires processing by inflammosome, TNF is transported to the cell surface where it is expressed as a plasma membrane protein and then cleaved by the protease TACE which releases mature TNF from the membrane)

31
Q

TNF release..

A

attracts neutrophils and stimulates phagocytosis

32
Q

IL-1b release…

A

causes t cell polarisation

33
Q

IL-6 release..

A

promotes neutrophil and b cell survival and proliferation, t cell polarisation

34
Q

IFNbeta release…

A

promotes IL-10 production by macrophages for antiviral responses

35
Q

IL_10 release…

A

inhibits TNF, IL-6 and IL-12 production by macrophages

36
Q

IL-12 release…

A

results in Th1 driven T cell responses and NK cell actviation

37
Q

Acute phase reaction (APR)

A

involves changes in plasma conc of specific proteins in response to inflammation
driven by cyotkines produced during localised inflam responses
systemic not localised reponses
changes due to altered protein synthesis in the liver
some acute proteins are increased whilst others are decreased

38
Q

acute phase proteins in preventing spread of infection

A

c reactive protein, SAP, complement proteins

39
Q

acute phase proteins in wound healing

A

fibrinogen, von willebrant factor, coagulation

40
Q

acute phase proteins in preventing systemic inflammation

A

c reactive protein, SAP, proteinase inhibitors, haptoglobin, manganese superoxide dismutase and serum amyloid A

41
Q

c reactive protein

A

mayor acute phase protein in humans
pentraxin (5 identical subunits)
used as a marker of inflammation
respond to IL-6 and IL-1beta hepatic expression by increasing in no dramatically

42
Q

T cell helper polarisation (2 steps)

A
  1. antigen presentation 0 antigens presented as MHC class 2 molecules on an antigen presenting cell recognised by t cell receptors of a naive CD4 t cell - this stimulates the t cell to proliferate
  2. polarisation - in response to cytokines secreted by the APC or other nearby immune cells, Th cell will polarise to take specific characteristics
43
Q

naive CD4 t cell proliferation in response to IL-12

A

Th1, promotes killing by macrophages, response to intracellular pathogens

44
Q

naive CD4 t cell proliferation in response to TGFbeta, IL-6, IL-1beta, IL-23

A

Th17, anti-fungal and anti-tumour immunity

45
Q

naive CD4 t cell proliferation in response to IL-4

A

Th2, promotes antibody production by B cells, anti-worm immune responses

46
Q

naive CD4 t cell proliferation in response to TGFbeta

A

Treg, immune suppressor

47
Q

what is autoimmune disease caused by

A

excessive production of pro-inflammitory cytokines

48
Q

autoinflammitory disorders

A

familial Mediterranean fever, noenatal onset multisystem inflam disease, TNF receptor-associated periodic syndrome, deficiency in IL/receptor antagonist, behcets disease
most result from genetic mutations that increase IL-1 production of signalling

49
Q

cytokine directed therapy

A

anti-TNF therapy, binds to TNF and stops its ability to produce cells - approved for RA, psoriasis, prosatic arthritis, chrons disease, ulcerative colitis and ankylosing spondylitis

50
Q

IL-1ra anti-inflammitory cytokine

A

binds to the IL-1 receptor but does not activate intracellular signalling - it is a competitive inhibitor of Il-1

Immunology (10 decks)

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