CAMs in Cutaneous Lupus Erythematosus

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Different patterns of ICAM-1 expression in the epidermis have been documented in LE vs other cutaneous inflammation and also between subsets of LE. In experimentally UVA- and UVB-induced lesions in patients with LE and PLE, those with SCLE showed ICAM-1 expression throughout the epidermis, those with DLE showed basal ICAM-1 staining, and those with PLE showed focal basal ICAM-1 staining associated with lymphocyte infiltrates (Stephansson and Ros 1993). SCLE, erythema multiforme, and lichen planus showed diffuse ICAM-1 expression throughout the epidermis in SCLE, basal and focal suprabasal ICAM-1 expression in erythema multiforme, and ICAM-1 expression on basal keratinocytes in lichen planus.Virus, UVB, and perhaps other triggers of cytokine release or possibly of ICAM-1 directly were suggested to explain these different ICAM-1 expression patterns (Bennion et al. 1995). Another group found no significant differences in CAM expression patterns in biopsy samples from spontaneous CCLE and SCLE lesions; they found ICAM-1 expression on keratinocytes, dermal inflammatory cells, and endothelial cells in the LE lesions (Tebbe et al. 1994).

Endothelial VCAM-1 staining was increased in biopsy samples from LE lesions compared with scleroderma and morphea (Jones et al. 1996), and increased expression of VCAM-1 has been found in nonlesional skin in patients with SLE and correlated to disease activity (Belmont et al. 1994). Activated endothelium, perhaps associated with increased endothelial expression of nitric oxide synthase, has been proposed as a unifying hypothesis for the diverse nature of SLE vascular lesions (Bel-mont and Abramson 1997). Patients with LE display aberrant kinetics and a prolonged time course of the epidermal expression of inducible nitric oxide synthase after UV provocation (Kuhn et al. 1998).

To study possible differences in CAM expression in PLE vs different subsets of CLE, photoprovocation and serial biopsy samples were studied (Hasan et al. 1997, Nyberg et al. 1997,Nyberg et al. 1999).We found different expression patterns of ICAM-1,VCAM-1,and E-selectin in patients with SLE and SCLE compared with patients with DLE and patients with PLE in our serial biopsy samples from evolving UV-induced reactions (Figs. 19.1-19.5). Transient vs persistent skin reactions revealed differences especially regarding ICAM-1 expression by day 7. It is possible that these early differences indicate different control mechanisms in different UV radiation-induced skin lesions. Negative control of ICAM-1 is associated with the f-actin cytoskeleton network, and disruption of f-actin enhances cytokine-induced ICAM-1 transcription (Trefzer and Krutmann 1995). A possible interpretation of the findings that patients with SLE and SCLE show linear expression of ICAM-1 in the whole epidermis whereas patients with DLE show mostly focal,basal staining is that UV irradiation plays a more direct role in the induction of ICAM-1 in SLE and SCLE. In DLE, cytokines such as IFN-Y and TNF-a released from the dermal infiltrate on UV irradiation are more likely to

Figs. 19.1-19.5. Examples of expression patterns of cellular adhesion molecules (CAMs) in UV-induced skin lesions in patients with cutaneous lupus erythematosus (CLE). Cryostat sections, mouse monoclonal antibodies against intercellular adhesion molecule-1 (ICAM-1), E-selectin, and vascular adhesion molecule-1 (VCAM-1) (Vectastain Elite ABC)

Fig. 19.1. Basal expression of ICAM-1 on kera-tinocytes and increased expression in the folli-cular epithelium. Endothelial cells and scattered inflammatory cells in the upper dermis express ICAM-1. UV-induced CLE lesion in a patient with chronic CLE (X250)

Fig. 19.2. Intense, bandlike ICAM-1 expression in the whole epidermis. UV-induced lesion in subacute CLE (X250)

Fig. 19.3. Lymphocyte function-associated antigen 1-positive lymphocytes accumulating around hair follicle. UV-induced lesion in a patient with chronic CLE (x250)

Fig. 19.4. E-selectin expression on upper dermal vessels. Staining is seen also without surrounding infiltrate. UV-induced lesion in a patient with chronic CLE (x250)
Figurate Erythema Dermatology

Fig. 19.5. VCAM-1 positive endothelial cells and some infiltrating cells in a patient with chronic CLE 14 days after UVB photoprovocation (x250)

induce the up-regulation of ICAM-1. Most UVB wavelengths do not penetrate the epidermis, and yet UVB induces reactions in the skin of patients with CCLE, perhaps indicating a role for the isomerization of trans- to cis urocanic acid, and the concomitant release of TNF-a. However,the cis-form of urocanic acid was found to be lower in light-protected skin of patients with DLE compared with patients with PLE and controls (Hasan et al. 1999). Our impression of biopsy samples from induced lesions in patients with LE is that the E-selectin-positive vessels are mostly found in upper and mid-der-mis (data not shown). Endothelial CAMs were up-regulated also in nonlesional skin of our patients with LE in accordance with earlier studies in which it was suggested t hat activated endothelial cells are a common denominator for the diverse symptoms in LE (Belmont et al. 1994). VLA-4 (the counterreceptor for VCAM-1) and lymphocyte function-associated antigen 1 (the counterreceptor for ICAM-1) have been reported to be overexpressed on lymphocytes from patients with SLE, VLA-4 only in patients with vasculitis (Tsokos 1996).

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