dr. Ahmad Garli, Sp.KK
DEFENISIKulit adalah organ penting dalam sistem imunitas terutama yang paling berperan adalah imunitas seluler. Imunitas kulit terdiri dari :1. Sistem fungsional2. Imunogenetik3. Struktur selBarrier kulit adalah penting dalam sistem non imunologik.
STRUKTUR SEL :1.Langerhans sel yang berasal dari sumsum tulang adalah sel yang paling penting dalam imunitas2.T limfosit :HelperDelayed type hipersensitivityCytotoxicSupresor
3.Mast sel, yang melepas histamine dan molekul vaso aktif4.Keratonisit, yang menghasilkan sitokines
SISTEM FUNGSIONAL :Skin-associated lymphoid tissuePeran dari aliran limfe dan limfonodes dan pembuluh darah dalam sistem imunologi.Fungsi komplemen yang bersifat lysis opsonization, granulisasi dan kemotaksis dari netrofil dan makrofag.
IMUNOGENETIK :Adanya HLA genes cluster reaksi.
Hypersensitivity dari pada kulit adalah reaksi yang berlebihan yang menyebabkan kerusakan dari pada jaringan. Ada 4 tipe, yaitu :1. Type I (immediete)2. Type II (antibody-dependdent cytotoxicity)3.Type III (immuno complex desease)4. Type IV (cell mediated or delayed)
Type I (immediate)
IgE is bound to the surface of mast cells by Fc receptors. On encountering antigen (e.g. housedust mite, food or pollen) the IgE molecules become crosslinked, producing degranulation and the release of inflammatory mediators. These include preformed mediators (such as histamine) and newly formed ones (e.g. prostaglandins or leukotrienes) The result in the skin is urticaria. although massive histamine release can cause anaphylaxis. The response occurs within minutes. although a delayed component is recognized. Factors other than IgE can cause mast cell degranulation.
Type II (antibody-dependent cytotoxicity)
Antibodies directed against an antigen on target skin cells or structures induce cytotoxic by killer T cells or by complement activation. For example. lgG pemphigus antibodies directed against desmoglein on the keratinocyte surface result in activation of complement. attraction of effector cells and the lysis of the keratinocytes Intra epidermal blisters result. Haemolytic anaemia and transfusion reactions are other examples of type II hypersensitivity. Some of these conditions are autoimmune
Type Ill (immune complex disease)
Immune complexes formed by the combination of antigen and antibodies in the blood are deposited in the walls of small vessels, often those of the skin. Complement activation, platelet aggregation and the release of lysosomal enzymes from polymorphs cause vascular damage. This leucocytoclastic vasculitis is seen with, for example, systemic lupus erythematosus and dermatomyositis, but also occurs with microbial infections such as infective endocarditis. The Arthus reaction is due to immune complex formation at a local site. It can be induced in the skin by an intradermal injection, and is maximal at 4-10 hours after injection.
Type IV (cell-mediated or delayed)
Specifically sensitized Th lymphocytes have secondary contact with the antigen when it is presented on the surface of antigen-presenting cells (APC). Cytokine release produces T cell activation and amplifies the reaction by recruiting other T cells and macrophages to the site. Tissue damage results which is maximal at 48-72 hours. Allergic contact dermatitis (see p. 30) and the tuberculin reaction to intradermally administered antigen are both forms of type IV reaction. The responses to skin infections such as leprosy or tuberculosis are granulomatous variants of the reaction.
Immunology1. Skin Provides a Physical Barrier to infection2. Langerhans cells form outposts of the cellular immune system and can resent antigens to immunocompeten cells e.g. T lymphocytes 3. T cells circulate through normal skin and form part of the skin-associated lymphoid tissue. They are localized by adhesion molecules
4. Keratinocytes can be immunologically active cells5. All four types of hypersensitivity reaction occur in the skin6. Genetic factors modulate immunological responses. Certain HLA antigens are associated with increased risk of skin disease