Immunohistochemical analysis of inflammation in primary sclerosing cholangitis

Objectives There are only limited data about the nature of the mononuclear infiltrate surrounding the affected biliary canaliculi in primary sclerosin g cholangitis (PSC). The aim of this study was to characterize the composit ion of the mononuclear infiltrate and to detect signs of activation/prolife ration among the various subpopulations involved. Furthermore the putative role of the biliary epithelium as antigen presenting cells (APC) was assess ed. Methods Liver biopsies of 14 PSC patients were analysed. Seven liver specim ens of non-inflammatory liver disease (NIL) patients with hepatocellular ca rcinoma or metastasis from colorectal carcinoma, as well as eight liver bio psies of primary biliary cirrhosis (PBC) patients, served as controls. Para ffin embedded material was stained with GB7, anti-CD3, anti-CD20, anti-CD45 RO, Deep frozen sections were stained with anti-CD4, anti-CD8, anti-CD25, a nti-CD86, anti-HLA-DR, anti-IFN gamma, anti-IL4, anti-ICAM1 and anti-alpha 4 beta 7, Stainings were scored by two pathologists using a semiquantitativ e scale. Results The portal infiltrate was found to consist mainly of CD3+CD45RO+ ce lls. Few cells expressed activation or proliferation markers in any of the liver specimens. In the PSC-material, significantly more of the infiltrativ e lymphocytes were positive for the integrin alpha 4 beta 7, as compared to hardly any positive cells in the NIL-group (P < 0.001) and <10% in the PBC -specimens (P < 0.01), Variable HLA-DR expression of the biliary epithelium was observed in all groups, however, without co-expression of ICAM1 or B7. 2. Conclusions The portal infiltrate in PSC liver histology specimens appears to consist mainly of non-activated memory T-lymphocytes, a substantial prop ortion of which expresses the gut-homing integrin alpha 4 beta 7, An antige n-presenting role for the biliary epithelium could not be demonstrated. Eur J Gastroenterol Hepatol 11:769-774 (C) 1999 Lippincott Williams & Wilkins.