Hertoghe sign

Epidermal hyperplasia. Hyperproliferation

of the epidermis can occur due to a number of causes,
as manifested in diseases such as psoriasis (pictured), as
well as lichen simplex chronicus, atopic dermatitis, lichen
planus, and verruca vulgaris.

In atopic dermatitis (see Chapter 14), LL-37 is downregulated,

probably due to the effect of the T2 cytokines
IL-4 and IL-13, which renders atopic skin more
susceptible to skin infections with, for example, S.
aureus, vaccinia virus (eczema vaccinatum), or herpes
simplex virus (HSV) (eczema herpeticum).10,12,13
Furthermore, patients with rosacea have been found
to possess high levels of aberrantly processed forms
of cathelicidin peptides (due to posttranslational processing
by stratum corneum tryptic enzyme), which
contributes to the increased inflammation in the skin.18
Cathelicidin can also form complexes with self-DNA,
which promotes activation of TLR9 on plasmacytoid
dendritic cells in the dermis, resulting in enhanced
cutaneous inflammation that contributes to psoriasis
pathogenesis.19

In the epidermis of atopic dermatitis (AD) skin, the

emergence of inflammatory dendritic epidermal cells
(IDECs) has been well documented.333 They are characterized
by the expression of CD1a, CD1b, CD1c,
CD11c, FceRI, CD23, HLA-DR, CD11b, CD206 (MMR/
macrophage mannose receptor), and CD36.333,334 In
situ staining of costimulatory molecules on epidermal
CD1a+
DC in AD skin showed that mainly cells
with the phenotype of IDEC display CD80 and CD86,
whereas Langerin+
CD1a+
epidermal LC are almost
devoid of these molecules.335 CD86 signaling is critical
for the stimulatory capacity of IDEC. Evidence exists
that, upon engagement of FceRI on IDEC, an immune