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week 2 lec 1 Flashcards

1
Q

layers of the epidermis from most superficial to deep

A

CLGSB

stratum corner
stratum lucidum
stratum granulosum
stratum spinosum
stratum basale

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2
Q

most superficial layer of epidermis

A

stratum croneum

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3
Q

function of stratum corneum

A

prevent microbe penetration, mechanical protection, prevent dehydration

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4
Q

what is stratum corner made up

A

dead skin cells with keratin and filaggrin (form macrofibrils)

held together by tight junctions and desmosomes

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5
Q

where is stratum lucidum found

A

thick skin: palms, soles, digits

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6
Q

function and cells in stratum lucidum

A

protection and dead cells (like stratum corneum; its just below it)

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7
Q

cells of stratum granulosum

A

living cells with keratin and fillagrin

lamellar granules - lipid rich layered granules that help reduce water loss

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8
Q

thickest layer of epidermis

A

stratum spinosum

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9
Q

which epidermis layer is keratin, proto-fillagrin and proteins synthesized

A

stratum spinosum

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10
Q

what are thicker bundles of keratin called and linked to?

A

Thick bundles of keratin called tonofibrils are linked to desmosomes

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11
Q

deepest epidermal layer

A

stratum basale

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12
Q

where are the stem cells for the epidermis

A

stratum basale

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13
Q

function of stratum basale

A

-melanocytes
-sensory receptors
-resident immune cells; langerhans cells

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14
Q

2 dermal layers

A

papillary layer (superficial)
reticular layer

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15
Q

whats in the papillary layer of the dermis

A

loose CT with elastic fibers, type III and I collagen

papilla; vascularized fingers to extend into and interlock with epidermis

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16
Q

reticular layer of dermis CT type

A

dense irregular CT- type 2 collagen

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17
Q

thickest layer of skin

A

reticular layer of dermis

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18
Q

reticular vs papillary layer of dermis CT

A

papillary- loose CT with elastic fibers, type III and I collagen

reticular- dense irregular CT with elastic fibers, type I collagen

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19
Q

reticular layer of dermis contrains

A

▪ Hair follicles, sensory receptors
▪ Nerves, arteries, veins, and lymphatics
▪ Sebaceous and sudoriferous (sweat) glands
▪ Smooth muscle cells, some adipose tissue

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20
Q

T cell activation steps

A

T cell receptor interacts with HLA2 on APC (antigen presenting cell)

CD4 co-receptor interacts with HLA-2

costimulatory interaction: CD28 (T cell) and CD80 (or 86) on APC

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21
Q

T cell polarization slide 11 chart

A

i.e. IL2 and TGF beta turn into T reg cell which then secretes IL 10 and TGF beta

I.e. IL 12 turns into TF cell

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22
Q

3 types of innate lymphoid cells (ILCs)

A

NK cells
NKT cells
resident ILCs

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23
Q

NK cells

A

cytotoxic monitor of
and responder to abnormal-looking or stressed cells

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24
Q

3 types of ILCs

A

type 1: Th1 cell development and type 1 response

type 2: Th2 cell delvopment and type 2 response

type 3: effective against extracellular bacteria, also contribute to lymphoid tissue development at the barrier

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25
Q

ILCs and cytokines

A

ILC1: secrete IFNy and TNFa

ILC2: secrete IL-4. IL-5, IL-9, IL-13

ILC3: secrete IL-22, IL-17, IFN-y

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26
Q

ILCs are derived from

A

lymphoid lineage (not myeloid)

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27
Q

what activates ILCs

A

ILC1= IL-12, IL-2

ILC2= alarmins, IL-2

ILC3= IL-1 beta, IL-23

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28
Q

what is IL-2 secreted by

A

Th cells

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29
Q

what is alarmin needed for

A

ILC2 type 2 response

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30
Q

alarming get released when

A

PRRs are activated on barrier tissue of epithelial cells

aka early-release cytokine

31
Q

ILC2 alarmins

A

IL-25, IL-33, TSLP

32
Q

IL-25, IL-33, TSLP (alarmins) push the barrier tissue to

A

secrete TH2-type cytokines

33
Q

ILC-2 cells secrete IL-17, IL22 to get a

A

Th17 like response

34
Q

what supports ILC activation and survivla

35
Q

mast cells are derived from

A

granulocyte-monocyte progenitors

36
Q

where do mast cells mature

A

in peripheral tissues that they migrate to (leave the bone marrow undifferentiated)

37
Q

what promotes survival and migration of mast cells

wat inhibits it

A

survive: high IgE circulating, IL-4, IL-33

die: IFN-y

38
Q

how long do mast cells live for

A

months in CT of barrier (ie.. dermis)

39
Q

in the presence of an allergen –> IgE from B cells sensitizes mast cells and lead to what

A

degranulation causing an allergic rxn: histamine, serotonin, heparin, proteases, IL-4, TNF-alpha

40
Q

mast cell activity steps

A
  1. recruit mast cell to tissue
  2. sensitize (PRRs, activating cytokines)
    –> receptors for IgE or express HLA-2 (APC)
  3. stimulus causes degranulation (acute i.e. allergic rhinitis, atopic dermatitis) then chronic type II inflammation, IgE, C3a and C5a, PRR
  4. 3 options: fully resolve, type II inflammation, or repair or fibrosis (via pro fibrotic growth factors)
41
Q

mast cells in what type of inflammation

A

type II- Atopic dermatitis, allergic rhinitis, asthma, food allergies

42
Q

mast cells to defend against

A

parasites, worms, venoms

43
Q

mast cells aren’t always pro-infalmamtory

A

proteases that degrade cytokines

IL-4 cause macrophages to do tissue repair

44
Q

eosinophils are derived from

A

myeloid lineage

45
Q

what cytokines causes proliferation and activation of eosinophils

46
Q

what causes migration of eosinophils from blood to peripheral tissue

A

eotaxin

and alarmins that activate ILC-2 cells (TSLP, IL33, IL25)

47
Q

eosinophils accumulate in what type of inflammation

A

acute, chronic type II and atherosclerotic plaques

48
Q

length of eosinophils

A

days; short lived

49
Q

granule content in eosinophils

A

major basic protein
- cationic protein (degranulation of mast cells, activate complement, increase membrane permeability)

eosinophil peroxidase (free radical generator)

cytokines- IL-4, IL-13, TNF alpha (pro inflam)
- sometimes IL-10 (anti-inflam)

50
Q

1st responders to inflammation

A

neutrophils

51
Q

neutrophils length

A

short lived; 12 hours- a couple days

52
Q

neurotphil functions

A

phagocytosis, release mediators, NETs

53
Q

whats in neutrophil granules

A

defensins and cathelicidins –> pores form –> lysis

cathepsin (target microbes)

lysozyme (glyocoside hydrolase to kill gram + bacteria)

lactoferrin (iron-binding protein interfere with iron metabolism in microbes)

myeloperoxidase (free radicals to attack phagosome)

54
Q

what is a NET

A

neutrophil extraceullar trap

-when neutrophils lyse and release their DNA into ECF

get bacteria trapped in the chromatin

histones are toxic got bacteria

55
Q

classic vs alternative macrophage activation

A

classic: induced by microbial products and IFNy which causes phagocytes, destroy microbes and inflammation

alternative: induced by IL13 and IL4 which causes tissue repair and anti-inflammatory

56
Q

innate immune réponse

A

NK cells and type 1 IFNs

if inadquedate then do adaptive immune reponse

57
Q

type 1 interferons

A

innate immune to viral infection ; paracrine and autocrine

IFNa and IFNb

58
Q

NK cells activated by

A

type 1 interferons

59
Q

NK cell activated

A

receptor mediated apoptosis via fas-fas ligand interaction

secrete perforin and granzyme (holes in membrane and granzyme also activates BH3 apoptotic protein bid and caspase 3)

60
Q

PRRs that bind PAMPs on bacteria

A

TLRs

lectin, glucan extracellular receptors

NOD-like receptors

RIG-like receptors

61
Q

innate immune functions of the skin

A
  • physical barrier via tight junctions in stratum corneum, fillagrin to prevent moisture loss, low pH, keratinocytes secrete AMPs (i.e. defensin)

keratinocytes direct immune response via TLRs and RIGs and release cytokines, alamrins (for ILCs) and chemokine)

62
Q

types of psoriasis

A
  • plaque psoriasis (most common)

guttate psoriasis

pusturlar psoriasis

63
Q

where is plaque psoriasis found

A

extensors, scalp, palms, soles

also nail involvement

64
Q

plaque psoriasis appearance

A

Well-demarcated salmon-pink papules or plaques with a silvery-white scale that will bleed if picked off

65
Q

onset of psoriasis

A

adolescent- early adulthood

66
Q

guttate psoriasis location and causes

A

trunk/abdomen

precipitated by streptococcal infection

67
Q

pustular psoriasis location

A

palms and soles

68
Q

psoriasis from what cytokines

A

dendritic cells that secrete IL-23

Th-17 cells (IL-17, recruit neutrophils, AMPs, cell proliferation of keratinocytes)

ILC-3 (IL-17)

69
Q

allergic contact dermatitis

A

non-anaphylactic and non-atopic “skin allergy” to something
▪ i.e. poison ivy, nickel, cosmetics

70
Q

clinical features of allergic contact dermatitis

A

48 hours - days after exposure –> well-demarcated erythema
and edema and ITCHING

if chronic exposure then lichenification, scales, crust, erosions…

71
Q

pathogenesis of allergic contact dermatitis

A

TLR and inflmmasome mediated activation of APC and T cells

72
Q

what mediated allergic contact dermatitis

A

hapten (sticks to normal skin cells and make it look foreign –> adaptive immune response against host cells)

hapten also activates inflammasome –> IL-1 secretions –> TH activated

73
Q

adaptive immune réponse in allergic contact dermattiis

A

cytotoxic T cells and CD8 memory cells, dermal dendritic cells…

BMS250 (47 decks)

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