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Skin as a protection against environmental threats. Antti Lauerma, M.D., Ph.D. Chief Medical Officer FIOH Dermatology Figures: copyright Blackwell (Rook, Textbook of Dermatology). SKIN AS ORGAN. Surface area 1.5 - 2 m2 Weight ~10% of body weight Purpose: To protect body against:

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Skin as a protection against environmental threats

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Skin as a protection against environmental threats l.jpg

Skin as a protection against environmental threats

Antti Lauerma, M.D., Ph.D.

Chief Medical Officer

FIOH Dermatology

Figures: copyright Blackwell (Rook, Textbook of Dermatology)


Skin as organ l.jpg

SKIN AS ORGAN

  • Surface area 1.5 - 2 m2

  • Weight ~10% of body weight

  • Purpose: To protect body against:

    • Mechanical stress

    • Physical damage

    • Pathogens

    • Foreign biologic material

    • Foreign nonbiologic material


Skin three levels of protection l.jpg

SKIN: THREE LEVELS OF PROTECTION

  • Mechanical barrier (stratum corneum)

  • Innate immunity

  • Acquired immunity


Stratum corneum l.jpg

STRATUM CORNEUM

  • The outer-most layer of skin

  • Approximately 10 cell layers thick

  • Consists of corneocytes and extracellular matrix

  • Protective layer against water loss from body


Stratum corneum damage l.jpg

STRATUM CORNEUM DAMAGE

  • EXOGENOUS DAMAGE

    • excess washing (toxic hand dermatitis)

  • ENDOGENOUS DAMAGE

    • inflammation

  • STRUCTURAL DAMAGE

    • atopic skin


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STRATUM CORNEUM REPAIR

  • Lipid synthesis in corneocytes

  • Lipid synthesis in keratinocytes

  • Basal keratinocyte proliferation


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STRATUM CORNEUM REPAIR (2)

  • Ointment/cream application

  • UV light therapy

  • Systemic retinoid use???


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Coombs-Gell I

  • Mast cells release histamine

  • Vasodilatation

  • Leakage of water to skin

  • Intense pruritus

  • 15 min - 2 hours (immediate hypersensitivity)


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Coombs-Gell II

  • Cytotoxic response

  • Macrophage-mediated killing of unfit cells

  • 24 hours

  • Erythema multiforme


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Coombs-Gell III

  • Antibody-antigen complexes

  • Complexes trapped at capillaries

  • Exanthema

  • 8-24 hours


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Coombs-Gell IV

  • APC presents antigen

  • T-cell mediated cellular inflammation

  • Allergic contact dermatitis

  • 24-48 hours (delayed hypersensitivity)


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INNATE IMMUNITY IN SKIN - START

  • Damage - danger signal

  • Preformed IL-1a released from KC

  • IL-1a stimulates KC to produce IL-1b, IL-6, TNFa and more IL-1a

  • TOLL receptors have same effect as IL-1a, sharing NF-kappa-beta signalling


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Arrival of Granulocytes

  • Larger vessel - lower speed

  • Attachment via P- and E-selectins

  • Movement to dermis through CXC -chemokine gradient

  • Proteases enable movement through ECM

  • Entrance to epidermis, movement through epidermis (”zipper movement”)


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Granulocytes in epidermis

  • Presence of IL-1, IL-6, TNF-a, GM-CSF, IFNg induce a respiratory burst in granulocytes

  • C3R, FCg receptors bind to microbes with opsonins (part of complement) to microbes

  • 1 bacteria/min, total over 50 bacteria per granulocyte


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Turn off the inflammation or call in the lymphocytes?

  • Keratinocytes produce IL-10, IL1ra, aMSH.

  • FB, MF, Lymphocytes produce TGF-beta:

    • IFN down

    • T cell anergy

    • Endoth. Cell Chk, adh mol down


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Turn off the inflammation or call in the lymphocytes?

  • Inflammation over 24-35 hours starts acquired immunity

  • Endothelial cells produce ICAM, VCAM

  • T cells adhere to endothelial cells and enter skin via chemokine (CC, not CXC) gradient


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Lymphocytes in the skin

  • Professional APC present antigen in the context of MHC II and B7.1/B7.2 to T cells.

  • (If keratinocytes present antigen, anergy results (no B 7.1/7.2))

  • IFNg, IFNa, TNFa, and LPS, bacterial cell wall, CpG induce MF and DC to produce IL-12

  • IL-12 favors Th1 response

  • Th1 T cells produce more IFNg that keeps up production of CC-chemokines


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What if ”danger” persists???

  • Inflammatory area will be isolated from surrounding tissue

  • IL-4 and IL-10 induce giant cells from MF

  • TGF beta stimulates action of giant cells and FB

  • Granulomatous inflammation


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