ATOPIC DERMATITIS: EPIDEMIOLOGY &
PATHOGENESIS
- A chronically relapsing skin disease
- Occurs mostly during early infancy
and childhood
- Abnormalities in barrier function,
allergen sensitization and recurrent
skin infections
 EPIDEMIOLOGY
- 10-20% prevalence in children in
US and other industrialized
countries
- Affects patients in both developed
and developing countries
- Female preponderance, 1.3:1.0
- Potential risk factors: small family
size, increased income and
education both in whites and
blacks, migration from rural to
urban environments and increased
use of antibiotics.
 DECREASED SKIN BARRIER FUNCTION
o Downregulation of cornified
envelope genes(FILAGGRIN),
reduced ceramide levels, increased
levels of endogenous proteolytic
enzymes, enhanced transepidermal
water loss.
o Epidermal changes likely contribute
to increased allergen absorption
into the skin and microbial
colonization.
o Decreased skin barrier acts as a site
for allergen sensitization and
predispose children to the
development of food allergy and
respiratory allergy.
 IMMUNOPATHOLOGY
o Acute eczematous lesions: marked
intercellular edema of the
epidermis.
o Dendritic antigen-presenting cells
exhibit surface bound IgE
molecules.
o Dermis of acute lesion: Influx of T
cells with occasional monocyte-
macrophages. CD3, CD4, CD45
o Eosinophils are rarely present in
Acute AD. Increased in chronic AD*
o Neutrophils are absent in AD skin
lesions even with S. aureus
colonization.
o Chronic lichenified lesions:
hyperplastic epidermis with
elongation of the rete ridges,
prominent hyperkeratosis, and
minimal spongiosis.
 CYTOKINES AND CHEMOKINES
o Acute AD: production of Th2
cytokines, IL4 and IL13*
o IL4- inflammatory pruritic lesion
similar to AD in mice
o IL31- induces severe pruritus and
dermatitis. Serum levels correlates
with the severity of the disease.
o Chronic AD: increase production of
IL-5, involved in eosinophil
development and survival.
o Increased production of
granulocyte macrophage CSF:
inhibits apoptosis of monocytes,
persistence of AD.
o Production of Th1 cytokines IL-12
and IL-18, IL-11 and TGF-1
o Interferon inducible protein 10,
monokine induced by IFN are
strongly upregulated in
keratinocytes and result in Th1 cell
migration toward epidermis
 T CELLS
o presence of Th2-like T cells in acute
AD produce cytokines that enhance
allergic skin inflammation.
o During the chronic phase of AD,
there is a switch to Th1-like cells
that primarily produce IFN-γ.
o Th1-like cells induce the activation
and apoptosis of keratinocytes
o Th17 cells produces IL-17.
o host defense by inducing
keratinocytes to produce
antimicrobial peptides as well as
promote neutrophil chemotaxis

 KERATINOCYTES

o AD keratinocytes secrete a unique

profile of chemokines and cytokines
after exposure to proinflammatory
cytokines.
o AD keratinocytes produce reduced
amounts of antimicrobial peptides
and this may predispose such
individuals to skin colonization and
infection with S. aureus, viruses,
and fungi.*