Soluble CAMs

Circulating, soluble isoforms of CAMs are biologically active in that they retain their binding function (Seth et al. 1991). It is regarded as most likely that the circulating forms of ICAM-1 and E-selectin are proteolytically cleaved at the cell membrane (Leeuwenberg et al. 1992). Possible physiologic roles for soluble CAMs are inhibition of binding by competition, or that the shedding of surface molecules is a process that serves to down-regulate the adhesion of the relevant ligand (Gearing and Newman 1993, Trefzer and Krutmann 1995).

Elevated levels of soluble (s)E-selectin were found in serum samples from 25 patients with active, widespread CLE lesions and without systemic symptoms. Most patients had a history of PLE (Nyberg 1997, Nyberg and Stephansson 1999, Nyberg et al. 1997). E-selectin is a specific marker for activated endothelial cells, which indicates that endothelial cells play a more central role in CLE than previously assumed. E-selectin is mainly expressed on the luminar surface of cytokine-activated endothelium, only in postcapillary venules but not by arterioles (Walsh et al. 1990). Hence, the conflicting results reported on (s)E-selectin in patients with vasculitis (Mrowka and Sieberth 1994, Spronk et al. 1994) can be due to involvement of vessels with different calibers.

Increased levels of sICAM-1 and sVCAM-1 were found in patients with SLE and SCLE (Nyberg 1997, Nyberg and Stephansson 1999). Increased levels of VCAM-1 in SLE serum have been reported by several authors and have been correlated to disease activity (Mrowka and Sieberth 1994,1995). In one study,VCAM-1 levels were elevated in patients with SLE and also in patients with DLE, although to a lesser extent than in those with SLE (Koide et al. 1996).

Soluble E-selectin might be useful clinically as an activity marker in CLE. Blocking of (s)E-selectin might be considered as possible therapy. An analogy is treatment with anti-ICAM-1 antibody that has decreased the rejection of skin grafts in experimental animal models (Trefzer and Krutmann 1995) and prevented neurologic symptoms and vasculitic skin lesions in SLE-prone mice (Brey et al. 1997).

Hypothetically, an altered CAM expression, induced by an unbalanced cytokine network brought about by an altered T-cell/B-cell repertoire in genetically susceptible individuals, could be a unifying concept for the related studies. It is possible, that studies of CAMs or certain subsets of T cells are useful in the evaluation of clinically doubtful, sunlight-induced cutaneous reactions.

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