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DA adalah penyakit peradangan kulit yang pruritik hasil dari interaksi kompleks antara

kerentanan genetic menimbulkan kecacatan sawar kulit, kecacatan pada system imunitas bawaan
dan peningkatan respon imun terhadap allergen dan antigen mikroba.

Eosinofil pada lesi kronis : sitolisis  protein granul dilepas ke dalam upper dermis lesi
Protein dasar major ekstraseluler (eosinophil-derived) dapat dideteksi dalam pattern fibrillar
sepanjang dermis atas (upper dermis)
Eosinofil diperkirakan menyumbang kepada allergic inflammation dengan mensekresi sitokin
dan mediator yang augment allergic inflammation dan menginduksi tissue injury pada DA
melalui produksi reactive oxygen intermediate dan pelepasan protein granul yang toksik.

The skin-specific chemokine, cutaneous T cellattracting


chemokine [CTACK; CC chemokine ligand
27 (CCL27)], is highly upregulated in AD and preferentially
attracts skin homing cutaneous lymphoid
antigen (CLA)CC chemokine receptor 10(CCR10)
T cells into the skin.17 CCR4 expressed on skin homing
CLAT cells can also bind to CCL17 on the vascular
endothelium of cutaneous venules. Selective
recruitment of CCR4-expressing Th2 cells is mediated
by macrophage-derived chemokine and thymus
and activation-
regulated cytokine, both of which are
increased in AD. Severity of AD has been linked to
the magnitude of thymus and activation-regulated
cytokine levels. In addition, chemokines such as fractalkine,
interferon (IFN)--inducible protein 10, and
monokine induced by IFN-are strongly upregulated
in keratinocytes and result in Th1-cell migration
toward epidermis, particularly in chronic AD.
Increased expression of the CC chemokines, macrophage
chemoattractant protein-4, eotaxin, and RANTES
(regulated on activation, normal T cell expressed
and secreted) contribute to infiltration of macrophages,
eosinophils, and T cells into both acute and
chronic AD skin lesions.