dr. Ahmad Garli, Sp.

KK

DEFENISI
Kulit adalah organ penting dalam sistem
imunitas terutama yang paling berperan adalah
imunitas seluler. Imunitas kulit terdiri dari :
1. Sistem fungsional
2. Imunogenetik
3. Struktur sel
Barrier kulit adalah penting dalam sistem non
imunologik.

STRUKTUR SEL :
1. Langerhans sel yang berasal dari
sumsum tulang adalah sel yang paling
penting dalam imunitas
2. T limfosit :
Helper
Delayed type hipersensitivity
Cytotoxic
Supresor

3. Mast sel, yang melepas histamine dan

molekul vaso aktif
4. Keratonisit, yang menghasilkan
sitokines

SISTEM FUNGSIONAL :
Skin-associated lymphoid tissue
Peran 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.

Immunology
1. Skin Provides a Physical Barrier to infection
2. 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

cells
5. All four types of hypersensitivity reaction
occur in the skin
6. Genetic factors modulate immunological
responses. Certain HLA antigens are
associated with increased risk of skin
disease