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84 Cards in this Set

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Describe the host defense properties of skin, including both innate and specific defenses.
--
These 2 barriers are the two major surfaces by which most microbes (Ags) enter body:
skin
mucous membranes
The epidermis has live _______ and dead cells with keratin which are renewed every 15-30 days. Microbes are sloughed off with old tissue
keratinocytes
When damaged keritinocyts secrete ____,_____, & _____. These inflammatory mediators
are chemotactic and enhance adhesion on dermal endothelial cells
IL-8, IL-1 and tumor necrosis factor (TNFa)
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 ________
UV damage
Dermis contains this type of glands which secretes oil that can coat microbes
sebaceous glands –
These cells that exist normally in the epidermis, constitutively express MHC class II, and fx to move Ags to LN
Langerhans cells (DC)
These lymphocytes exist intraepithelially in the epidermal layer and function in skin defence.
T cells
Normal flora can inhibit pathogenic microbes. Two examples are _______ enzymes which restrict growth of viruses and _______ which
inhibit other bacteria
restriction
bacteriocins
Why are skin transplants often autologous?
--
immediate rejection of tissue is called a hyperacute rejection and is mediated by ________
antibodies
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
Autograft
Types of tissue grafts:
This describes when tissue transferred from genetically identical individuals (monozygotic twins)
Isograft
Types of tissue grafts:
This describes when tissue is transferred between genetically distinct individuals of the same species. Genetic differences can result in rejection
Allograft
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.
Xenograft
Graft rejection is due to ________ and ______ .
specificity
memory
This rejection is due to the primary immune response. It takes 1-2 weeks for immunological recognition and rejection.
First set rejection
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)
Second set rejection
______ play a central role in graft rejection
T cells
in graft rejection what Tcell/s are most important (CD4,CD8,bothCD4/CD8)
bothCD4/CD8>CD4>CD8
When performing an allograft, what cell markers must one evaluate. Why?
--
the ______codes for proteins that play the biggest role in graft survival
MHC loci
the “major” histocompatible antigens
Class __ MHC matches are more important than class __ matches
II
I
Even if you completely match MHC, you still usually have to use immunosuppression due to these
minor histocompatibility antigens -
matches of the Ag on this tissue type are the other major factor for graft success
blood type
What cell types play a role in graft rejection?
--
In the effector phase of graft rejection, it is this cell that can be cytotoxic
CD4+
What can be done to increase the success of an allograft transplantation?
--
Immunosuppression for graft survival:
These drugs prevent T and B cell proliferation. They are often given just before and after transplant.
mitotic inhibitors
Immunosuppression for graft survival:
These drugs are given as anti-inflammatory agents
corticosteriods
Immunosuppression for graft survival:
These drugs provide specific immunosuppression in that they prevent T cell activation by blocking IL-2 and IL-2R transcription
fungal metabolites (e.g., cyclosporin A and FK506)
Immunosuppression for graft survival:
These drugs provide specific immunosuppression in that they treat donor and/or graft tissue
Antibodies

e.g.,
anti-CD3
anti-CD25 (high-affinity IL-2R)
anti-CD20 (B cells)
CTLA4-Ig – block co-stimulation/induce suppression
7. What is the immunological basis for the four types of hypersensitivity (e.g. what immunological factors cause the pathology)?
--
Type I (immediate type) is Ig__ mediated
E
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)
Type I (immediate type)
atopic eczema (a/k/a atopic dermatitis) has similarities to what other chronic condition
chronic asthma
those with atopic eczema (a/k/a atopic dermititis) have a characteristic thickening of the __________
basement membrane
Those with atopic eczema (a/k/a atopic dermatitis)
have increased ___ and ________ levels in blood and increased ____ cytokines in skin
IgE
eosinophil
Th2
patients with atopic eczema often have recurrent skin infections with diseases like _______ due to “skewed”
immune response
impetigo (infection with Staph or Strep)
This hypersensitivity is a type of autoimmunity. It occurs when the body creates Abs directed against self
Type II hypersensitivity (cytotoxic)
give the "equasion" for Type II (cytotoxic) hypersensitivity
Ab (often IgG) on a cell + C’ = cell lysis
In this dz example of Type II (cytotoxic) hypersensitivity, IgG against type IV collagen affects the kidneys and lungs
Goodpasture’s syndrome
In Goodpasture’s syndrome the damage is due to ___, _____ (inflammation) and _____(ADCC)
C’
PMNs
NK cells
Type III hypersensitivity is involves these
immune complex
give the "equasion" for Type III hypersensitivity
Ab + Ag = complexes = C’ activation
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)
Arthus reaction
common illnesses due type III hypersensitive reactions
SLE
skin vasculitis
Type IV hypersensitivity is this type of hypersensitivity.
delayed type hypersensitivity, DTH
Type IV hypersensitivity is mediated by this type of cells
CD4+
An example of Type IV hypersensitivity used diagnostically
Mantoux skin test (tuberculin skin test)
In the Mantoux skin test this is diagnostic
size of induration
pt exposed to poison ivy has this type of delayed type hypersensitivity, DTH
Contact hypersensitivity
type II, III sensitivities involve these Abs
IgM, IgG
type-I(anaphylactic)
characteristics:
antibody?
antigen?
response time?
appearance?
histology?
transferred with?
examples?
IgE
exogenous
15-30 minutes
weal & flare
basophils and eosinophil
antibody
allergic asthma, hay fever
type-II(cytotoxic)
characteristics:
antibody?
antigen?
response time?
appearance?
histology?
transferred with?
examples?
IgG, IgM
cell surface
minutes-hours
lysis and necrosis
antibody and complement
antibody
erythroblastosis fetalis, Goodpasture's nephritis
type-III(immune complex)
characteristics:
antibody?
antigen?
response time?
appearance?
histology?
transferred with?
examples?
IgG, IgM
soluble
3-8 hours
erythema and edema, necrosis
complement and neutrophils
antibody
SLE, farmer's lung disease
 
type-IV(delayed type)
characteristics:
antibody?
antigen?
response time?
appearance?
histology?
transferred with?
examples?
None
tissues & organs
48-72 hours
erythema and induration
monocytes and lymphocytes
T-cells
tuberculin test, poison ivy, granuloma
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?
Pemphigus vulgaris
How do you dx Pemphigus vulgaris?
ELISA for the presence of autoantibodies to DESMOGLEINS
(anti-Dsg3=mucosal)
(anti-Dsg1=skin)
How do you tx Pemphigus vulgaris?
corticosteroids
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.
Pemphigus foliaceus
what test should you run to dx Pemphigus foliaceus
anti-Dsg1 autoantibodies
not anti-dsg3 autoantibodies
Bullous diseases:
IgG and/or C3 in basement membrane (immunofluorescence microscopy)
Auto-Abs against basement membrane proteins
DQb2*0301
Bullous pemphigoid
Bullous diseases:
granular deposits of IgA (autoAbs against epidermal transglutaminase)
Strict gluten-free diet reduces “flare-ups”
90% patients with B8/DRw3 and DQw2
Dermatitis herpetiformis (DH)
similar pathology to DH
linear deposits of IgA (and often C3) along basement membrane (immunofluorescence)
autoantibodies against basement membrane proteins
Linear IgA disease
give 3 systemic autoimmune diseases with cutaneous features
Systemic lupus erythematosis
Scleroderma
Psoriasis
25 y/o african american women presents with fever, weakness, arthritis, skin rashes (butterfly rash over cheeks), kidney dysfunction, etc. What is the dx
Lupus
is lupus a local or systemic dz
systemic
in lupus these lead C’ lysis of cells, inflammation
damage to blood vessels (kidney) – organ damage
immune complexes
In lupus IgG and C’ proteins associated with epidermal basement membrane leads to _____ which causes a butterfly rash on the cheeks
inflammation
Pt presents with thickening of skin & small sausage shaped fingers. What do you suspect?
Scleroderma
This dz involves cold-induced blanching of fingers and may precede scleroderma symptoms
Raynaud’s phenomenon
Give 3 types of scleroderma
CREST
Diffuse disease
Linear/morphea
CREST scleroderma accounts for 80% of cases. What does CREST stand for:
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)
Describe diffuse sclerodermal disease
more severe (kidney, lung damage)
Describe Linear/morphea sclerodermal disease –
pathology limited to the skin
How do you dx scleroderma
Autoantibodies

may find ANA, anti-centromere Abs (50%), scleroderma antibodies (SCL-70; 30%), anti-topoisomerase Abs
Scleroderma Therapy
treat symptoms
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
Psoriasis
_________ may be the cause of skin cell proliferation in psoriasis(not conclusive)
T cell cytokines
type of NHL that localizes to the skin
Cutaneous T cell lymphoma (CTCL)
Types of CTCL
Mycosis fungoides
Sezary syndrome
In this type of CTCL mushroom like skin lesions develop. Cancer cells stay localized to the skin (not in blood)
Mycosis fungoides
In this type of CTCL, large areas of skin are affected. You also find cancer cells in the blood and LNs
Sezary syndrome