EXPRESSION OF CELL-ADHESION MOLECULES IN TUBULOINTERSTITIAL NEPHRITISASSOCIATED WITH SJOGRENS-SYNDROME

The tissue distribution of cellular adhesion molecules (ICAM-1. ELAM-1 . VCAM-1) was studied in specimens from sis normal human kidneys and i n six biopsies from kidneys with tubulointerstitial nephritis associat ed with Sjogren's syndrome. In addition, the expression of cellular ad hesion molecules was examined both in four renal biopsies from cases o f tubulointerstitial nephritis of di verse pathogenesis and in six lip biopsies from cases of Sjogren's syndrome, ICAM-1 was expressed on va scular endothelial cells in normal kidneys. in all specimens of tubulo interstitial nephritis and in salivary glands, On tubular epithelial c ells, ICAM-1 appeared slightly in normal kidneys: otherwise tubular ep ithelial ICAM-1 was observed in and around the foci of cellular infilt ration in all cases of tubulointerstitial nephritis, ELAM-1 and VCAM-1 were observed on the newly generated vessels in massive cellular infi ltrates in some cases of tubulointerstitial nephritis associated with Sjogren's syndrome; by contrast, they were not seen in normal kidneys and in cases of tubulointerstitial nephritis of diverse pathogenesis. In the lip biopsies from salivary glands, ICAM-1 was observed on ducta l epithelial cells in and around the foci of cellular infiltration, an d ELAM-1 and VCAM-1 occasionally appeared on the newly generated vesse ls in massive cellular infiltrates. Chronic and progressive inflammati on may be facilitated by such ELAM-1 and VCAM-1 expression on newly ge nerated vessels. The adhesion molecules were thought to play a role in the pathogenesis of tubulointerstitial nephritis and sialoadenitis as sociated with Sjogren's syndrome, It was thus concluded that the same inflammatory process that took place in the salivary glands to induce the characteristic tissue change of Sjogren's syndrome likely was oper ative in the renal tubulointerstitial tissue as well.