Skin as an insurance against ecological dangers.


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SKIN AS ORGAN. Surface territory 1.5 - 2 m2Weight ~10% of body weightPurpose: To ensure body against:Mechanical stressPhysical damagePathogensForeign biologic materialForeign nonbiologic material. SKIN: THREE LEVELS OF PROTECTION . Mechanical boundary (stratum corneum)Innate immunityAcquired invulnerability.
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Skin as an insurance against natural dangers Antti Lauerma, M.D., Ph.D. Boss Medical Officer FIOH Dermatology Figures: copyright Blackwell (Rook, Textbook of Dermatology)

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SKIN AS ORGAN Surface territory 1.5 - 2 m2 Weight ~10% of body weight Purpose: To secure body against: Mechanical anxiety Physical harm Pathogens Foreign biologic material Foreign nonbiologic material

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SKIN: THREE LEVELS OF PROTECTION Mechanical obstruction (stratum corneum) Innate resistance Acquired insusceptibility

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STRATUM CORNEUM The external most layer of skin Approximately 10 cell layers thick Consists of corneocytes and extracellular lattice Protective layer against water misfortune from body

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STRATUM CORNEUM DAMAGE EXOGENOUS DAMAGE abundance washing (dangerous hand dermatitis) ENDOGENOUS DAMAGE aggravation STRUCTURAL DAMAGE atopic skin

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STRATUM CORNEUM REPAIR Lipid blend in corneocytes Lipid union in keratinocytes Basal keratinocyte expansion

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STRATUM CORNEUM REPAIR (2) Ointment/cream application UV light treatment Systemic retinoid use???

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Coombs-Gell I Mast cells discharge histamine Vasodilatation Leakage of water to skin Intense pruritus 15 min - 2 hours (quick extreme touchiness)

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Coombs-Gell II Cytotoxic reaction Macrophage-interceded killing of unfit cells 24 hours Erythema multiforme

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Coombs-Gell III Antibody-antigen edifices Complexes caught at vessels Exanthema 8-24 hours

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Coombs-Gell IV APC presents antigen T-cell intervened cell irritation Allergic contact dermatitis 24-48 hours (postponed excessive touchiness)

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INNATE IMMUNITY IN SKIN - START Damage - peril signal Preformed IL-1a discharged from KC IL-1a invigorates KC to create IL-1b, IL-6, TNFa and more IL-1a TOLL receptors have same impact as IL-1a, sharing NF-kappa-beta flagging

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Arrival of Granulocytes Larger vessel - lower speed Attachment by means of P-and E-selectins Movement to dermis through CXC - chemokine angle Proteases empower development through ECM Entrance to epidermis, development through epidermis ("zipper development")

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Granulocytes in epidermis Presence of IL-1, IL-6, TNF-a, GM-CSF, IFNg instigate a respiratory burst in granulocytes C3R, FCg receptors tie to microorganisms with opsonins (a portion of supplement) to organisms 1 microscopic organisms/min, complete more than 50 microbes for every granulocyte

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Turn off the aggravation or bring 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 irritation or bring in the lymphocytes? Irritation more than 24-35 hours begins obtained resistance Endothelial cells produce ICAM, VCAM T cells stick to endothelial cells and enter skin through chemokine (CC, not CXC) slope

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Lymphocytes in the skin Professional APC present antigen with regards to MHC II and B7.1/B7.2 to T cells. (In the event that keratinocytes present antigen, anergy comes about (no B 7.1/7.2)) IFNg, IFNa, TNFa, and LPS, bacterial cell divider, CpG prompt MF and DC to create IL-12 IL-12 favors Th1 reaction Th1 T cells deliver more IFNg that keeps up generation of CC-chemokines

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What if "threat" holds on??? Incendiary zone will be disengaged from encompassing tissue IL-4 and IL-10 instigate monster cells from MF TGF beta animates activity of goliath cells and FB Granulomatous irritation

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