Interface dermatitis

Characteristic histological pattern of a diffuse, superficial dermatitis, which is detectable in etiopathogenetically different inflammatory dermatoses.

Interface dermatitis is characterized by an epitheliotropic, lymphocytic infiltrate that leads to chronic, vacuolar damage to the basal keratinocytes (and melanocytes) in the epidermis, with signs of apoptosis and its histomorphologically detectable consequences.

The term "lichenoid dermatitis" is also used synonymously with the term "interface dermatitis". This refers terminologically to lichen ruber and is to be understood as a subgroup of interface dermatitis.

Diseases whose histological substrate is characterized by interface dermatitis (varies n. El Shabrawi-Caelen u. Soyer):

• Interface dermatitis - Lichen planus-like interface dermatitis with dense band-like infiltrate and premature terminal differentiation with distinct stratum granulosum:
  • Lichen planus and variants
  • Erythema dyschromicum perstans (Ashy dermatosis)
  • Lichen nitidus
  • Drug exanthema, lichenoides
  • Dermatomyositis
  • Keratosis lichenoides chronica
  • Lichenoid graft-versus-host disease
  • Lupus erythematosus chronicus discoides
  • Lichen striatus.
• Interface dermatitis with acute cytotoxic damage (erythema exsudativum-multiforme-like interface dermatitis); marked basal hydropic damage to the surface epithelium with necrotic keratinocytes in all epithelial layers:
  • Erythema exsudativum multiforme
  • Stevens-Johnson syndrome
  • Toxic epidermal necrolysis
  • Acute lupus erythematosus
  • Drug reaction, fixed
  • Erythema dyschromicum perstans
  • Acute cytotoxic dermatitis after chemotherapy
  • Phototoxic dermatitis
  • Pityriasis lichenoides chronica
  • Pemphigus, paraneoplastic.
• Interface dermatitis with psoriasiform epidermal hyperplasia:
  • Lichenoid purpura
  • Lichen striatus
  • Porokeratosis mibelli
  • Secondary syphilis
  • Acrodermatitis chronica atrophicans (early stage)
  • Mycosis fungoides
  • Drug reaction, adverse.
• Interface dermatitis with irregular epidermal hyperplasia:
  • Verrucous lichen planus
  • Verrucous discoid lupus erythematosus.
  • Verrucous lichenoid drug reaction.
• Interface dermatitis with epidermal atrophy (usually only minor inflammatory infiltrates):
  • Acrodermatitis chronica atrophicans
  • Lichen sclerosus et atrophicus
  • Atrophic lichen ruber
  • Poikiloderma
  • Lichenoid actinic keratoses

Interface dermatitis (lichenoid tissue reaction) is a histopathologic pattern reflecting a distinct cytotoxic immune response that occurs in a number of clinically diverse inflammatory skin diseases, of which lichen planus and cutaneous lupus erythematosus are considered prototypical.

All interface dermatitides should be understood as a specific immune reaction directed against specific antigens of the basal epidermis. However, the reaction is likely to be functionally different in nature. Thus, in autoimmune diseases, it is directed against versch. In autoimmune diseases it is directed against various autoantigens, e.g. in lupus erythematosus in particular against nuclear structures such as SSA/Ro, which are increasingly expressed under inflammatory stimulation.

• In anti-viral forms of interface dermatitis, virus-infected cells are recognized and attacked cellularly.
• In lichenoid actinic keratosis, the immune response is directed against tumor antigens, such as the UV-mutated epitopes of p 53.
• In drug interface dermatitis, as observed in Stevens-Johnson syndrome, immunogenic neo-antigens are present in the epidermis due to covalent binding of drugs or their metabolites.

Thus, the wide spectrum of diseases associated with the picture of interface dermatitis raises doubts that a common pathomechanism underlies this histologic pattern.

The essence of this response is invasion of the basal epidermis by cytotoxic immune cells, with recruitment of effector cells by local activation of the interferon system with expression of INF-regulated chemokines. The initial inflammatory response is triggered by cytotoxic immune cells expressing CXC chemokine receptor 3 and lesional keratinocytes producing corresponding ligands, CXCL motif ligands 9/10/11. The histological signature of this particular response is characterized by apoptotic keratinocytes, with various apoptosis mechanisms involved, such as the perforin/granzyme system used primarily by cytotoxic CD8+ T cells.

The signs of apoptosis of keratinocytes are described as "dyskeratotic" or as "single cell necrosis". Light microscopic structure-poor, eosinophilic corpuscles remain at the dermo-epidermal junctional zone also described as:

• cytoid corpuscles
• Civatte-bodies
• hyaline corpuscles
• colloid bodies

referred to as. These apoptotic keratinocytes "drip" into the papillary body in advanced stages of interface dermatitis. They are then referred to as "civatte bodies." Pigment also drips into the papillary body (pigment incontinence) and is taken up there by macrophages (melanophages).

Other relevant apoptosis factors of the lichenoid reaction are FAS/CD95- as well as the TNF-alpha/TRAIL- mechanisms.

The signs of apoptosis of keratinocytes are described as "dyskeratotic" or "single cell necrosis". Eosinophilic corpuscles with little structure remain at the dermo-epidermal junction zone even as:

• cytoid corpuscles
• Civatte-bodies
• hyaline bodies
• Colloidal body

is called.

1. Braegelmann C et al (2021) Immunostimulatory Endogenous Nucleic Acids Perpetuate Interface Dermatitis-Translation of Pathogenic Fundamentals Into an In Vitro Model. Front Immunol 11:622511.
2. El Shabrawi-Caelen L, Soyer H-P (2003) Inflammatory dermatoses of the dermoepidermal junction (interface dermatitis). In: Histopathology of the skin. Kerl H et al (eds) Springer Verlag, Berlin Heidelberg New York, p 117.
3. Khudhur AS et al. (2014) Oral lichenoid tissue reactions: diagnosis and classification. Expert Rev Mol Diagn14:169-184.
4. Scholtissek B et al (2011) Immunostimulatory Endogenous Nucleic Acids Drive the Lesional Inflammation in Cutaneous Lupus Erythematosus. J Invest Dermatol 137:1484-1492