Immunoelectron microscopic observations on the inflammatory infiltrates and HLA antigens in hepatitis B and non-A, Non-B

Abstract

The present knowledge of the inflammatory reaction occurring in situ during hepatitis B favors a T cell-dependent MHC-restricted immune response. However, the reports in the literature are primarily based on the application of monoclonal antibodies directed at different lymphocyte subsets which discern only lymphocytic phenotypes and do not reflect the actual situation adequately. Therefore, we investigated the liver biopsies of patients with hepatitis B (28 patients) and non-A, non-B (21 patients) by immunoelectron microscopy with monoclonal antibodies directed at lymphocyte subtypes (pan-B, pan-T, T8, T4 and NKH1) and at activation epitopes (IL-2 receptor, TA1 and T11/3) as well, in order to determine the phenotype in association with the activation status of the lymphocytes that are in close contact with hepatocytes; thus, establishing an effector-target cell relationship on the ultrastructural level. We were able to confirm the central role of T8 lymphocytes being the predominant type of lymphocytes in close contact with liver cells in the space of Disse. A certain percentage of these cells expressed "activation" markers as IL-2 receptor, TA1 and T11/3. In acute hepatitis, the NK lymphocytes made up a fifth of all lymphocytes, whereas their number dropped below 10% in the chronic stage. There was a vague correlation between the inflammatory activity of the disease and the expression of HLA antigens (both classes I and II) on inflammatory cells and also on hepatocytes. The results did not show significant differences between hepatitis B and non-A, non-B.(ABSTRACT TRUNCATED AT 250 WORDS)

Murine liver antigen presenting cells control suppressor activity of CD4+CD25+ regulatory T cells

“…1). In inflammatory states of the liver, hepatocytes can upregulate MHC class II 6 and consequently gain the ability to interact with CD4 ϩ T cells and Treg too. In addition to LSEC and KC, we found that hepatocytes also induce suppressive activity of Treg (Fig.…”

“…1 Indeed, the most prevalent professional APC in liver, liver sinusoidal endothelial cells (LSEC) and Kupffer cells (KC), 2,3 have been shown to actively induce immune tolerance. 2,4,5 In addition, hepatocytes, which can upregulate expression of class II molecules of the major histocompatibility complex (MHC II) during hepatitis 6 and may then serve as APC for CD4 ϩ T lymphocytes, 7 also have been implicated in the induction of immune tolerance. 8 Nevertheless, rapid infiltration of the liver with inflammatory cells is induced during infection.…”

Sublobular veins as the main site of lymphocyte adhesion/transmigration and adhesion molecule expression in the porto-sinusoidal-hepatic venous system during concanavalin A-induced hepatitis in mice

“…At 1,4,6,24, and 48 hours after Con A injection, the liver was perfused first with phosphate buffered saline for 30 seconds and then with either 2% paraformaldehyde in 0.1 mol/L phosphate buffer, pH 7.4, or 1.5% glutaraldehyde in 0.067 mol/L cacodylate buffer, pH 7.4, plus 1% sucrose for 3 minutes via the portal vein. A part of the liver specimen was immersed in 10% formalin for 1 week, and serial paraffin sections 4-µm thick were cut and stained with hematoxylin and eosin (H-E).…”

“…1,2 Lymphocyte attachment to the endothelial cells of central veins and portal veins, termed ''endothelialitis'', 3 and lymphocyte migration into the subendothelial layer are common features seen in inflammatory human liver diseases. 4 However, the mechanism and locational heterogeneity of lymphocyte adhesion and transmigration in the hepatic vasculature are poorly understood.…”

Interleukin-2-activated natural killer cells can induce both apoptosis and necrosis in rat hepatocytes

“…The number of NK cells is increased during the acute phase of hepatitis; however, during various chronic liver diseases, the NK cell population is diminished. [2][3][4]7 The importance of NK cells in the early stage of infection was demonstrated in NK-deficient mice (bg/bg mice) or mice depleted of NK cells by treatment with a specific antibody. These animals became more susceptible to murine cytomegalovirus infection.…”