Immuno

Front 1

Describe the host defense properties of skin, including both innate and specific defenses.

Back 1

--

Front 2

These 2 barriers are the two major surfaces by which most microbes (Ags) enter body:

Back 2

skin
mucous membranes

Front 3

The epidermis has live _______ and dead cells with keratin which are renewed every 15-30 days. Microbes are sloughed off with old tissue

Back 3

keratinocytes

Front 4

When damaged keritinocyts secrete ____,_____, & _____. These inflammatory mediators
are chemotactic and enhance adhesion on dermal endothelial cells

Back 4

IL-8, IL-1 and tumor necrosis factor (TNFa)

Front 5

Keratinocytes can also produce IL-12 or IL-10 in response to injury. IL-10 can also be inhibitory
may play a role in down-regulating immune responses following ________

Back 5

UV damage

Front 6

Dermis contains this type of glands which secretes oil that can coat microbes

Back 6

sebaceous glands –

Front 7

These cells that exist normally in the epidermis, constitutively express MHC class II, and fx to move Ags to LN

Back 7

Langerhans cells (DC)

Front 8

These lymphocytes exist intraepithelially in the epidermal layer and function in skin defence.

Back 8

T cells

Front 9

Normal flora can inhibit pathogenic microbes. Two examples are _______ enzymes which restrict growth of viruses and _______ which
inhibit other bacteria

Back 9

restriction
bacteriocins

Front 10

Why are skin transplants often autologous?

Back 10

--

Front 11

immediate rejection of tissue is called a hyperacute rejection and is mediated by ________

Back 11

antibodies

Front 12

Types of tissue grafts:
This describes when self tissue is transferred from one site to another in the same individual. e.g., skin for burn patient or
blood vessels to replace blocked coronary arteries

Back 12

Autograft

Front 13

Types of tissue grafts:
This describes when tissue transferred from genetically identical individuals (monozygotic twins)

Back 13

Isograft

Front 14

Types of tissue grafts:
This describes when tissue is transferred between genetically distinct individuals of the same species. Genetic differences can result in rejection

Back 14

Allograft

Front 15

Types of tissue grafts:
This describes when tissue is transferred between different species. This involves the greatest genetic variability and the greatest immune response. It is used only as a temporary solution.

Back 15

Xenograft

Front 16

Graft rejection is due to ________ and ______ .

Back 16

specificity
memory

Front 17

This rejection is due to the primary immune response. It takes 1-2 weeks for immunological recognition and rejection.

Back 17

First set rejection

Front 18

This rejection is due to memory response. If you put same tissue in the individual again, you will then see a quicker rejection (5-6 days)

Back 18

Second set rejection

Front 19

______ play a central role in graft rejection

Back 19

T cells

Front 20

in graft rejection what Tcell/s are most important (CD4,CD8,bothCD4/CD8)

Back 20

bothCD4/CD8>CD4>CD8

Front 21

When performing an allograft, what cell markers must one evaluate. Why?

Back 21

--

Front 22

the ______codes for proteins that play the biggest role in graft survival

Back 22

MHC loci
the “major” histocompatible antigens

Front 23

Class __ MHC matches are more important than class __ matches

Back 23

II
I

Front 24

Even if you completely match MHC, you still usually have to use immunosuppression due to these

Back 24

minor histocompatibility antigens -

Front 25

matches of the Ag on this tissue type are the other major factor for graft success

Back 25

blood type

Front 26

What cell types play a role in graft rejection?

Back 26

--

Front 27

In the effector phase of graft rejection, it is this cell that can be cytotoxic

Back 27

CD4+

Front 28

What can be done to increase the success of an allograft transplantation?

Back 28

--

Front 29

Immunosuppression for graft survival:
These drugs prevent T and B cell proliferation. They are often given just before and after transplant.

Back 29

mitotic inhibitors

Front 30

Immunosuppression for graft survival:
These drugs are given as anti-inflammatory agents

Back 30

corticosteriods

Front 31

Immunosuppression for graft survival:
These drugs provide specific immunosuppression in that they prevent T cell activation by blocking IL-2 and IL-2R transcription

Back 31

fungal metabolites (e.g., cyclosporin A and FK506)

Front 32

Immunosuppression for graft survival:
These drugs provide specific immunosuppression in that they treat donor and/or graft tissue

Back 32

Antibodies

e.g.,
anti-CD3
anti-CD25 (high-affinity IL-2R)
anti-CD20 (B cells)
CTLA4-Ig – block co-stimulation/induce suppression

Front 33

7. What is the immunological basis for the four types of hypersensitivity (e.g. what immunological factors cause the pathology)?

Back 33

--

Front 34

Type I (immediate type) is Ig__ mediated

Back 34

E

Front 35

this hypersensitivity type includes many skin allergies from acute temporary conditions like atopic urticaria (hives) to more concerning chronic conditions like atopic eczema (a/k/a atopic dermatitis)

Back 35

Type I (immediate type)

Front 36

atopic eczema (a/k/a atopic dermatitis) has similarities to what other chronic condition

Back 36

chronic asthma

Front 37

those with atopic eczema (a/k/a atopic dermititis) have a characteristic thickening of the __________

Back 37

basement membrane

Front 38

Those with atopic eczema (a/k/a atopic dermatitis)
have increased ___ and ________ levels in blood and increased ____ cytokines in skin

Back 38

IgE
eosinophil
Th2

Front 39

patients with atopic eczema often have recurrent skin infections with diseases like _______ due to “skewed”
immune response

Back 39

impetigo (infection with Staph or Strep)

Front 40

This hypersensitivity is a type of autoimmunity. It occurs when the body creates Abs directed against self

Back 40

Type II hypersensitivity (cytotoxic)

Front 41

give the "equasion" for Type II (cytotoxic) hypersensitivity

Back 41

Ab (often IgG) on a cell + C’ = cell lysis

Front 42

In this dz example of Type II (cytotoxic) hypersensitivity, IgG against type IV collagen affects the kidneys and lungs

Back 42

Goodpasture’s syndrome

Front 43

In Goodpasture’s syndrome the damage is due to ___, _____ (inflammation) and _____(ADCC)

Back 43

C’
PMNs
NK cells

Front 44

Type III hypersensitivity is involves these

Back 44

immune complex

Front 45

give the "equasion" for Type III hypersensitivity

Back 45

Ab + Ag = complexes = C’ activation

Front 46

This type III hypersensitivity reaction describes when Ag is injected into epidermal layer and inflammation is seen ~4 hours later (rather than immediatly)
You'll see “boggy edema” (due to Mf and PMNs)rather than a wheal and flare. You may see fibrinoid necrosis (due to destruction of capillaries)

Back 46

Arthus reaction

Front 47

common illnesses due type III hypersensitive reactions

Back 47

SLE
skin vasculitis

Front 48

Type IV hypersensitivity is this type of hypersensitivity.

Back 48

delayed type hypersensitivity, DTH

Front 49

Type IV hypersensitivity is mediated by this type of cells

Back 49

CD4+

Front 50

An example of Type IV hypersensitivity used diagnostically

Back 50

Mantoux skin test (tuberculin skin test)

Front 51

In the Mantoux skin test this is diagnostic

Back 51

size of induration

Front 52

pt exposed to poison ivy has this type of delayed type hypersensitivity, DTH

Back 52

Contact hypersensitivity

Front 53

type II, III sensitivities involve these Abs

Back 53

IgM, IgG

Front 54

type-I(anaphylactic)
characteristics:
antibody?
antigen?
response time?
appearance?
histology?
transferred with?
examples?

Back 54

IgE
exogenous
15-30 minutes
weal & flare
basophils and eosinophil
antibody
allergic asthma, hay fever

Front 55

type-II(cytotoxic)
characteristics:
antibody?
antigen?
response time?
appearance?
histology?
transferred with?
examples?

Back 55

IgG, IgM
cell surface
minutes-hours
lysis and necrosis
antibody and complement
antibody
erythroblastosis fetalis, Goodpasture's nephritis

Front 56

type-III(immune complex)
characteristics:
antibody?
antigen?
response time?
appearance?
histology?
transferred with?
examples?

Back 56

IgG, IgM
soluble
3-8 hours
erythema and edema, necrosis
complement and neutrophils
antibody
SLE, farmer's lung disease
 

Front 57

type-IV(delayed type)
characteristics:
antibody?
antigen?
response time?
appearance?
histology?
transferred with?
examples?

Back 57

None
tissues & organs
48-72 hours
erythema and induration
monocytes and lymphocytes
T-cells
tuberculin test, poison ivy, granuloma

Front 58

72 y/o man presents with blisters that began in the mouth and spread to other locations in the skin. He has a dz in which IgG antibodies to keratinocyte antigens (IgG + C’) leads to blister formation. He has DR4 & DRw6. What is the dz?

Back 58

Pemphigus vulgaris

Front 59

How do you dx Pemphigus vulgaris?

Back 59

ELISA for the presence of autoantibodies to DESMOGLEINS
(anti-Dsg3=mucosal)
(anti-Dsg1=skin)

Front 60

How do you tx Pemphigus vulgaris?

Back 60

corticosteroids

Front 61

65 south american man presents with blisters on skin but no blisters in mucosal membranes. He reports that the blisters get worse when he goes out in sunlight.

Back 61

Pemphigus foliaceus

Front 62

what test should you run to dx Pemphigus foliaceus

Back 62

anti-Dsg1 autoantibodies
not anti-dsg3 autoantibodies

Front 63

Bullous diseases:
IgG and/or C3 in basement membrane (immunofluorescence microscopy)
Auto-Abs against basement membrane proteins
DQb2*0301

Back 63

Bullous pemphigoid

Front 64

Bullous diseases:
granular deposits of IgA (autoAbs against epidermal transglutaminase)
Strict gluten-free diet reduces “flare-ups”
90% patients with B8/DRw3 and DQw2

Back 64

Dermatitis herpetiformis (DH)

Front 65

similar pathology to DH
linear deposits of IgA (and often C3) along basement membrane (immunofluorescence)
autoantibodies against basement membrane proteins

Back 65

Linear IgA disease

Front 66

give 3 systemic autoimmune diseases with cutaneous features

Back 66

Systemic lupus erythematosis
Scleroderma
Psoriasis

Front 67

25 y/o african american women presents with fever, weakness, arthritis, skin rashes (butterfly rash over cheeks), kidney dysfunction, etc. What is the dx

Back 67

Lupus

Front 68

is lupus a local or systemic dz

Back 68

systemic

Front 69

in lupus these lead C’ lysis of cells, inflammation
damage to blood vessels (kidney) – organ damage

Back 69

immune complexes

Front 70

In lupus IgG and C’ proteins associated with epidermal basement membrane leads to _____ which causes a butterfly rash on the cheeks

Back 70

inflammation

Front 71

Pt presents with thickening of skin & small sausage shaped fingers. What do you suspect?

Back 71

Scleroderma

Front 72

This dz involves cold-induced blanching of fingers and may precede scleroderma symptoms

Back 72

Raynaud’s phenomenon

Front 73

Give 3 types of scleroderma

Back 73

CREST
Diffuse disease
Linear/morphea

Front 74

CREST scleroderma accounts for 80% of cases. What does CREST stand for:

Back 74

calcinosis (lime salt deposits in tissues)
Raynaulds phenomenon
Esophageal involvement (shrinkage, poor movement of food anywhere along GI tract)
Sclerodactyly (hardening of the finger tips or toes)
Telangiectasia (dilated blood vessels)

Front 75

Describe diffuse sclerodermal disease

Back 75

more severe (kidney, lung damage)

Front 76

Describe Linear/morphea sclerodermal disease –

Back 76

pathology limited to the skin

Front 77

How do you dx scleroderma

Back 77

Autoantibodies

may find ANA, anti-centromere Abs (50%), scleroderma antibodies (SCL-70; 30%), anti-topoisomerase Abs

Front 78

Scleroderma Therapy

Back 78

treat symptoms

Front 79

Pt presents with a patch of excessive skin proliferation appearing as silvery scales on the skin of the elbow and knees. In addition he has nail pitting and arthritis. What is the dz

Back 79

Psoriasis

Front 80

_________ may be the cause of skin cell proliferation in psoriasis(not conclusive)

Back 80

T cell cytokines

Front 81

type of NHL that localizes to the skin

Back 81

Cutaneous T cell lymphoma (CTCL)

Front 82

Types of CTCL

Back 82

Mycosis fungoides
Sezary syndrome

Front 83

In this type of CTCL mushroom like skin lesions develop. Cancer cells stay localized to the skin (not in blood)

Back 83

Mycosis fungoides

Front 84

In this type of CTCL, large areas of skin are affected. You also find cancer cells in the blood and LNs

Back 84

Sezary syndrome