Lecture 33 - Immunology and skin

Question 1

Skin set up

Answer 1

Epidermis - made up of keratinocytes and melanocytes
Dermo-epidermal junction - proteins that stick these layers together
Dermis - blood vessels
Fat

Question 2

How can blisters form?

Answer 2

Keratinocytes are anchored by hemi desmosomes

-if make an antibody that weakens this adherence then get blisters

Question 3

Bullous pemphigoid

Answer 3

autoimmune disease due to the formation of igG antibodies against hemo-desmosomal proteins

-cognitive impairment due to multiple cerebrovascular accidents prior to onset of her skin problems

Blood brain barrier
-blood does not interact with neural tissue but if damaged, e.g stroke - then will get damage to blood vessels, then will get mixing of the blood and neural tissue

• different isoforms of bullous pemphigoid antigen - one in brain, skin and muscle
• if get damage of this blood brain barrier will get an immune repsonse agaisnt antigens that would not normally be exposed in blood, then make antibodies and will get get cross reactivity and get antibodies damaging skin so get blisters

Question 4

How to test for this?

Direct immunofluorescence

Answer 4

• want to see if keratinocytes are attatched to hemidesmosome
• give an antibody with a marker attatched, mix the skin sample together, and then shine fluoresent light on the skin
• if there is a band of fluoresence then this means there is a linear depsoit of igG at the dermo-epidermal junciton which is damaging the lining

Question 5

How are keratinocytes attatched to each other?

what is pemphigus vulgaris

Answer 5

• attatched to each other by desmosomes
• so if make an antibody against desomsomes - then get a flaky skin because epidermis is falling apart and get superficial erosions
• get this in the mouth - because there is a variant in the mouth

Can also look at direct immunofluoresence - and can see if igG antibodies are there

Question 6

Atopic eczema

Answer 6

• common condition in children
• in epidermis, profilaggrin is converted to filaggrin making a natural moisturising factor that helps to cement the brick wall together
• can get a mutation with this gene, and found that these people are far more likely to have atopic eczema
• as if there is none of the filaggrin, then will beable to get things get through the dermis layer easier

-can do patch testing

Question 7

Patch testing can be done

Answer 7

• can test different materials and see which one gets an immune response
• uses purified antigen to provoke the dermatitis on the back
• patient can avoid the antigen that is identified

Question 8

Allergic contact dermatitis

Answer 8

• Patients with atopic dermatitis can be more susceptible to allergic contact dermatitis
• defects in epidermal barrier may account for other allergins in atopic dermatitis

Question 9

Why are patients immunosuppressed?

Answer 9

1. to treat severe disease e.g use immunosupression drugs
2. Because of the disease - severe combined immunodeficiencey, HIV
3. due to organ transplantation - renal transplant, bone marrow transplant

Question 10

What should you do to make a diagnosis?

Answer 10

In clinic or wards, it is often better to treat clinically rather than waiting for results of tests as the disease can quickly become overwhelming

Swab for bacteria, virus
Skin biopsy for tissue culture

Question 11

Humman papilloma virus

Answer 11

can cause warts

• due to an inherited defect of cell mediated immunity
• patient can have an increase risk of cancer

Question 12

How can immunosupresison lead to cancer?

Answer 12

• due to immune cells being depleted e.g due to immunosupression and then they can no longer fight the cancer
• Squamous cell carcinoma
• Immuno surveillance repairs UV damage
• however when immunsupressed, then imparied UV damage repair

competent immune system is needed to prevent skin infection and cancer

Question 13

vitiligo

Answer 13

• immune reaction, lose colour of skin

- not much treatment