DECREASED STAINING OF HEPARAN-SULFATE IN NON-LESIONAL SKIN OF A SUBGROUP OF PATIENTS WITH SYSTEMIC LUPUS-ERYTHEMATOSUS

Heparan sulfate proteoglycans (HSPGs) are components of the basement m embrane of various tissues. They are composed of a core protein and of the negatively charged glycosaminoglycan side chain heparan sulfate, which is covalently bound to the core protein. We previously found tha t in both human and murine lupus nephritis, heparan sulfate staining i n the basement membrane of the glomerulus is almost completely absent, and that there was an inverse correlation between heparan sulfate sta ining and glomerular immunoglobulin deposits. As immunoglobulin deposi ts are also present in the skin of systemic lupus erythematosus patien ts, we investigated the heparan sulfate staining pattern in the baseme nt membrane of the dermal - epidermal junction. Furthermore, rye studi ed whether there was a correlation between heparan sulfate staining an d deposition of immunoglobulin in the basement membrane of this juncti on, and between heparan sulfate staining and the presence of anti-DNA antibodies in the serum.Biopsies of non-lesional skin of 21 systemic l upus erythematosus patients (15 anti-DNA positive and 6 anti-DNA negat ive patients at the time of biopsy) were stained for the HSPG-core pro tein (mAb JM-72), highly sulfated stretches within heparan sulfate (JM -13), the low sulfated regions of heparan sulfate (mAb JM-403) and for immunoglobulin depositions. Abnormal and discontinuous staining of th e low sulfated parts of heparan sulfate using mAb JM-403 in the baseme nt membrane was found in skin biopsies of 4 out of 15 systemic lupus e rythematosus patients with anti-DNA antibodies. In contrast, all speci mens of anti-DNA negative patients showed normal continuous staining, Staining with JM-13 and JM-72 showed normal linear staining in both gr oups. The decreased heparan sulfate staining was correlated significan tly with the presence of immunoglobulin deposits in the basement membr ane. The subgroup could not be identified by its clinical picture. Our results suggest similar but not identical pathways in systemic lupus erythematosus nephritis and skin of systemic lupus erythematosus patie nts.