PMID- 7616001
OWN - NLM
STAT- MEDLINE
DCOM- 19950822
LR  - 20190723
IS  - 0022-202X (Print)
IS  - 0022-202X (Linking)
VI  - 105
IP  - 1 Suppl
DP  - 1995 Jul
TI  - In three types of interface dermatitis, different patterns of expression of 
      intercellular adhesion molecule-1 (ICAM-1) indicate different triggers of 
      disease.
PG  - 71S-79S
AB  - We found distinct patterns of intercellular adhesion molecule-1 (ICAM-1) 
      expression in three diseases characterized by interface dermatitis with 
      mononuclear infiltrates and keratinocyte cytotoxicity: lichen planus (LP), 
      subacute cutaneous lupus erythematosus (SCLE), and erythema multiforme (EM). In 
      LP, basal keratinocytes show strong ICAM-1 expression associated with a dermal 
      infiltrate, but ICAM-1 expression in the rest of the epidermis is minimal. In 
      SCLE, there is diffuse epidermal ICAM-1 expression, sometimes with accentuation 
      on the cell surface of basal cells. In EM, there is strong basal cell expression 
      of ICAM-1 with evident cell surface accentuation, and also pockets of suprabasal 
      expression with cell surface accentuation. These patterns are associated with 
      different factors that trigger cytokine release in different locations. Both 
      tumor necrosis factor-alpha (TNF-alpha) and interferon-gamma (IFN-gamma) produce 
      greater relative ICAM-1 expression in basal keratinocytes than in more 
      differentiated keratinocytes. In LP, the pure basal keratinocyte expression of 
      ICAM-1 appears to be caused by cytokines, predominantly IFN-gamma, released by 
      dermal lymphocytes. The pattern of ICAM-1 in SCLE corresponds to the pattern 
      induced by ultraviolet radiation (UVR): diffuse epidermal ICAM-1 expression, 
      sometimes with basal accentuation. Some individuals are "responders" to TNF-alpha 
      or UVR, showing high levels of ICAM-1 expression following UVR or TNF-alpha 
      stimulation in vitro or UVR stimulation in vivo. We propose that the pattern of 
      ICAM-1 induction in SCLE is dependent on UVR-induced TNF-alpha release. EM is 
      associated with apparent latent Herpes simplex virus, and Herpes simplex virus 
      (HSV)-infected keratinocytes show enhanced ICAM-1 expression. We propose that in 
      EM suprabasal ICAM-1 expression may be induced directly by HSV infection or 
      indirectly through TNF-alpha release induced by HSV reactivation. Induction of 
      ICAM-1 within the epidermis is stratified and individually variable. Basal 
      keratinocytes show maximal induction of ICAM-1 expression due to innate 
      sensitivity to TNF and IFN-gamma stimulation, and to location adjacent to dermal 
      sources of cytokines. Suprabasal ICAM-1 can be induced by UVR and epidermal 
      TNF-alpha release, and by factors such as viral infection. Different triggers of 
      cytokine release and adhesion molecule induction may influence the different 
      patterns of inflammation seen in diverse inflammatory skin diseases.
FAU - Bennion, S D
AU  - Bennion SD
AD  - Department of Dermatology, Fitzsimons Army Medical Center, Denver, Colorado, USA.
FAU - Middleton, M H
AU  - Middleton MH
FAU - David-Bajar, K M
AU  - David-Bajar KM
FAU - Brice, S
AU  - Brice S
FAU - Norris, D A
AU  - Norris DA
LA  - eng
GR  - R01 AR26427/AR/NIAMS NIH HHS/United States
GR  - T32 AR07411/AR/NIAMS NIH HHS/United States
PT  - Journal Article
PT  - Research Support, U.S. Gov't, P.H.S.
PL  - United States
TA  - J Invest Dermatol
JT  - The Journal of investigative dermatology
JID - 0426720
RN  - 0 (Interleukin-1)
RN  - 0 (Tumor Necrosis Factor-alpha)
RN  - 126547-89-5 (Intercellular Adhesion Molecule-1)
SB  - IM
MH  - Erythema Multiforme/*metabolism/pathology
MH  - Humans
MH  - Intercellular Adhesion Molecule-1/*metabolism
MH  - Interleukin-1/pharmacology
MH  - Keratinocytes/metabolism
MH  - Lichen Planus/*metabolism/pathology
MH  - Lupus Erythematosus, Cutaneous/*metabolism/pathology
MH  - Simplexvirus/physiology
MH  - Tumor Necrosis Factor-alpha/pharmacology
MH  - Ultraviolet Rays
EDAT- 1995/07/01 00:00
MHDA- 1995/07/01 00:01
CRDT- 1995/07/01 00:00
PHST- 1995/07/01 00:00 [pubmed]
PHST- 1995/07/01 00:01 [medline]
PHST- 1995/07/01 00:00 [entrez]
AID - S0022-202X(15)42249-3 [pii]
AID - 10.1111/1523-1747.ep12316107 [doi]
PST - ppublish
SO  - J Invest Dermatol. 1995 Jul;105(1 Suppl):71S-79S. doi: 
      10.1111/1523-1747.ep12316107.