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Year 3 Sem 1 > Week 3 > Flashcards

Week 3 Flashcards

1
Q

where are CD40 and CD40L present?

A

CD40 - APC

CD40L - CD4 T cell

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2
Q

where are CD28 and CD80/86?

A

CD28 on T cell

CD80/86 on APC

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3
Q

which cytokine acts in an autocrine matter to promote T cell growth?

A

IL2 (3rd signal from APC)

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4
Q

which CD4 T cell provides CD40L?

A

Th1

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5
Q

which CD4 T cells are involved in IC and EC bacterial infections

A 
Th1 = IC
Th17= EC
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6
Q

what are the 3 steps in priming of CD8?

A

DC with increased expression of B7 activates CD8 directly
DC activates DC4 which in return enhances co-stimulatory activity in DC
activated CD4 cells secrete IL2 which directly acts on CD8

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7
Q

which cytokines to CTLs release?

A

IFNy (inhibits viral replication)

TNFa

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8
Q

what do the granules used in CTL contain and what do they target?

A

granules contain, perforin, granulysin, granzymes

intracellular targets include: caspases, nuclear DNA, mitochondrial proteins

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9
Q

how does acute and chronic inflammation differ? in terms of the cells involved

A

shift from polynuclear low nuclei cell (neutrophils)

to mononuclear cells (macrophages, lymphocytes)

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10
Q

what are the 3 outcomes of acute inflammation?

A

1- complete repair/ resolution
2- fibrosis/ scarring
3. progression to chronic inflammation

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11
Q

what does the recruitment of eosinophils depend on?

A

eotaxin - CC chemokine

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12
Q

causes of chronic inflammation?

A

persistent infection by IC bacteria
immune reactions- autoimmune
immune response to normal substances
prolonged exposure to toxic substances

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13
Q

role of macrophages in chronic inflammation?

A

produce cytokines that destroy pathogen and initiate repair
activated by cytokines from activated T cells
accumulation by increased recruitment of monocytes?

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14
Q

what is classical macrophage activation?

A

pro-inflammatory pathway
induced by microbial agents (endotoxin, IFNy)
activated macrophage produced lysosomal enzymes (NO, ROS) which enhances their ability to kill ingested organism and secrete cytokines

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15
Q

what is alternative macrophage activation?

A

anti-inflammatory
induced y IL4 and IL13 produced by T cells, mast cell and esinophils
role in tissue repair - secrete GF, increased angiogenesis, stimulate collagen synthesis

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16
Q

how do mast cells work in chronic inflammation?

A

express surface receptors that bind to Fc portion of IgE - degranulation and release of histamine

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17
Q

how do macrophages and lymphocytes work in a bidirectional way?`

A

macrophage displays Ag to T cell and produce cytokines which activates Tcell
activated T cell releases cytokines to recruit and activate macrophages which again leads to Ag presentation and more cytokine production to T cells

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18
Q

what does a granuloma consist of? whats its function?

A

macrophages
fibroblasts
giant cell (1 cell with multiple nuclei)
lymphocytes

it attempts to wall off substances it sees as foreign but is unable to eliminate it

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19
Q

function of epidermal GF?

A

mitogenic for keratinocytes and fibroblasts
stimulates keratinocyte maturation
stimulates formation of granulation tissue

20
Q

function of hepatocyte GF?

A

enhances proliferation of heptocytes

increases cell motility

21
Q

function of VEGF?

A

increased proliferation of endothelial cells

increases vascular permeability

22
Q

function of platelet derived GF? PDGF.

A

chemotactic for neutrophils, macrophages, fibroblasts and SMC
activates and stimulates proliferation of fibroblasts, endothelial cells
stimulates synthesis of ECM proteins

23
Q

function of fibroblast GF?

A

chemotactic and mitogenic for fibroblasts
stimulates angiogenesis
Stimulates ECM protein synthesis

24
Q

function of TGF-beta (transforming GF-B)

A

chemotactic for leukocytes and fibroblasts
stimulates ECM protein synthesis
suppresses acute inflammation

25
Q

where does VEGF come from?

A

mesenchymal cells

26
Q

where does PDGF come from?

A

platelets, macrophages, endothelial cells, SMC

27
Q

where does HGF come from?

A

fibroblasts, endothelial cells, stromal cells in liver

28
Q

where does EGF come from?

A

activated macrophages, keratinocytes and salivary glands

29
Q

where does FGF come from?

A

macrophages, mast cells, endothelial cells

30
Q

where does TGF-beta come form?

A

platelets, T cells, macrophages, endothelial cells, SMC, fibroblasts

31
Q

differentiate caseous and non-caseous granuloma/

A

caseous - infectious causes (TB, fungal)

non caseous - non-infectious causes - autoimmune disorders, RA, sarcoidosis

32
Q

what is healing by primary intention?

A

injury involves 1 epithelial layer

mechanism of repair is epithelial regeneration

33
Q

what is healing by secondary intention?

A

more extensive cell/ tissue loss

repair involved regeneration and scar formation

34
Q

what is positive selection?

A

T cells must recognize/ bind moderately to self MCH
apoptosis of those that do not interact with HLA molecules

recognize, pMHCI and pMHCII expressed by cortical eputhelial cells

35
Q

what is negative selection?

A

apoptosis of medullary thymocytes that recognize self peptide on MHC1/MHCII too strongly

36
Q

what is central tolerance?

A

negative selection

37
Q

what cells mediate positive selection?

A

cortical epithelial cells

38
Q

what cells mediate negative selection?

A

DC, macrophages of bone marrow origin

39
Q

how do effector T cells migrate from blood to tissues to perform their effecttor functions?

A

exit through LN efferent lymphatics or splenic vein and migrate into tissues to perform their effector functions

40
Q

what happens with peptide: MHC bind in T cells?

A

signal transduction occurs through signalling proteins associated with TCR
Ag binding leads to phosphorylation of signalling cascades of protein: protein interactions = increased expression of genes
IL2 is the first gene switched on = its acts on itself to promote T cell growth

41
Q

what cytokines do CTLs release?

A 
IFN-y= inhibits viral replication and activates macrophages
TNFa= recruitment of other inflammatory cells and promote target cell killing
42
Q

what are the functions of perforin, granzymes and ganulysin?

A

perforin: creating pores in target cells membrane
granzymes: enter cell via perforin
granulysin: creates holes in target cell membrane and destroy it

43
Q

what are acute phase proteins?

A

Acute-phase proteins are a class of proteins whose plasma concentrations increase or decrease in response to inflammation. This response is called the acute-phase reaction. For acute-phase reaction is characteristic fever, acceleration of peripherals leukocytes, circulating neutrophils and their precursors

44
Q

GF involved in liver regeneration?

A

TGFa and HGF

45
Q

what is the difference between central and effector memory cells?

A

central cells express CCR7 and remain in lymphoid tissues

effector memory cells lack CCR7 and migrate to tissues

Year 3 Sem 1 (12 decks)

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