Immunohistochemical Study of Adhesion Molecules in Liver Inflammation

Volpes, Riccardo; Oord, Joost J. van den; Desmet, Valeer

doi:10.1002/hep.1840120110

Cited by 200 publications

(79 citation statements)

References 52 publications

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“…1, 38,42 Intercellular adhesion molecule-1 (ICAM-1) molecules, whose ligand on T cells is LFA-1, are commonly present not only on professional APC, such as macrophages and DCs, but also on target cells involved in inflammatory processes. 43 They are absent in normal muscles, but are observed in all inflammatory myopathies, where they are expressed not only by the endothelium of perimysial arterioles and venules, but also by muscle fibres, especially the non-necrotic ones, which are invaded by mononuclear cells. 38,44,45 This distribution suggests that ICAM-1 is involved both in leukocyte-endothelium interactions and in cytotoxicity processes, where it contributes to killing efficiency by creating an intimate contact region in which cytotoxic factors can more easily induce the lethal hit on target cells.…”

Section: Muscle Cells Recruit Leukocytesmentioning

confidence: 99%

Skeletal muscle cells: from local inflammatory response to active immunity

et al. 2010

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The skeletal muscles are the major living component of the human body. They are constituted by stable cells, the myofibres, and by adult multipotent stem cells, the satellite cells, which can multiply to regenerate and repair the damaged tissues. Injections of DNA in muscle cells have been used to produce recombinant proteins with opposite goals: somatic reparation of genetic defects, which needs to elicit no inflammatory or immune response, and DNA vaccination, which needs a robust immune response. Because of possible therapeutical interventions, a growing body of information is being produced dealing with every aspect of the myofibres during inflammatory and autoimmune responses: skeletal muscle-antigen presenting cell (APC) interaction and intrinsic APC capabilities of myoblasts and myocytes, the response to released cytokines and their endogenous production, the regulation of Toll-like receptors and major histocompatibility complex expression. According to these data, the muscle tissue is now emerging no longer as a passive bystander, but more as an active player that, when correctly manipulated, can drive tolerance or immunization to these de novo produced proteins. In the present review, we summarize the recent developments on the control of muscle immune function.

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Section: Muscle Cells Recruit Leukocytesmentioning

confidence: 99%

Skeletal muscle cells: from local inflammatory response to active immunity

et al. 2010

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“…Moreover, ICAM-l cell surface expression has been reported in affected tissue in a variety of inflammatory disorders, including human liver allograft rejection [3]. viral hepatitis B [14,15] and autoimmune liver disease [15,16].…”

Section: Introductionmentioning

confidence: 99%

“…we also wished to determine basal and stimulated ICAM-I gene expression in freshly isolated PBMC from PBC palients compared with normal healthy individuals. Moreover, since hepatocytes are known to express ICAM-1 in liver inflammation [15] and because this may be an important factor in liver cell injury, we have examined the capacity of pro-inflammatory cytokines to induce ICAM-1 expression in primary cultures of human hepatocytes.…”

Section: Introductionmentioning

confidence: 99%

Circulating intercellular adhesion molecule-1 (ICAM-1) in autoimmune liver disease and evidence for the production of ICAM-1 by cytokine-stimulated human hepatocytes

Thomson

Satoh

Nüssler

et al. 1994

Clinical and Experimental Immunology

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SUMMARY A circulating form of the membrane‐bound ICAM‐1 (CD54). a ligand for lymphocyte function‐associated antigen‐1 (LFA‐I), has recently been identified in normal human scrum. In this study. scrum levels of soluble ICAM‐1 (sICAM‐1) were determined by sandwich ELISA both in normal healthy individuals of both sexes and in subjects with autoimmune liver diseases. Patients with primary biliary cirrhosis (PBC). primary sclerosing cholangitis and chronic active hepatitis (autoimnune) showed significant elevations in sICAM‐1 compared with normal healthy subjects. The median level in PBC was approximately seven‐fold above normal. Significant elevations in sICAM‐1 were also detected, however, in patients with inactive alcoholic cirrhosis, suggesting that impaired liver clearance might at least in part account for the increased serum levels seen in patients with autoimmune liver disease. In patients with PBC. sICAM‐I levels were related to summary assessment of disease severity (Child‐Pugh classification) and correlated significantly with serum biochemical indices of liver function, including measures both of cholestasis and liver cell injury. In contrast, serum levels of E‐selectin did not differ significantly from healthy controis. Although it has been suggested that peripheral blood mononuclear cells (PBMC) may be a source of sICAM‐I. investigation of ICAM‐I gene expression by reverse transcriptase polymerase chain reaction revealed similar basal levels of ICAM‐1 message in PBMC of normal individuals and those with active PBC. This suggests that PBMC may not be a significant source of sICAM‐1 in this disease. Similar increases in ICAM‐I mRNA expression were found in cultured, concanavalin A (Con A)‐stimulated lymphocytes of both PBC patients and controls. Significantly, stimulation of cultured, normal human hepatocytes with proinflammatory cytokines and endotoxin induced cell surface expression ofICAM‐1 and the secretion/shedding of sICAM‐1 into the hepatocyte culture medium. This new finding suggests that hepatocytes may bean important sourceofsICAM‐1 in autoimmune and other chronic liver diseases. The possible role of sICAM‐1 in inflammatory disorders remains to be determined.

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“…7 ICAM-1 has been implicated in liver transplant rejection by studies that show increased levels of soluble ICAM-1 during rejection episodes and histological detection of increased ICAM-1 during liver allograft rejection. [8][9][10] Parenchymal cells may constitutively express or may be induced to express adhesion molecules by various cytokines. However, the role of adhesion molecules in the presentation of major histocompatibility complex (MHC) antigens by parenchymal cells is not known.…”

mentioning

confidence: 99%

Efficacy of anti-intercellular adhesion molecule-1 immunotherapy on immune responses to allogeneic hepatocytes in mice

Bumgardner

Heininger

et al. 1998

Hepatology

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Adhesion molecules appear to play important roles in vascularized organ allograft rejection, because antibodies directed against them are effective in prolonging survival of vascularized organ allografts in rodents. However, the efficacy of these agents for cellular allografts is unknown. The current studies were undertaken to determine the role of intercellular adhesion molecule-1 (ICAM-1) and vascular cell adhesion molecule-1 (VCAM-1) on host immune responses to purified hepatocytes. Host mice (C3H, H-2 k ) grafted with hepatocytes in sponge matrix allografts (HC-SMA) received IgG isotype control, anti-ICAM-1, or anti-VCAM-1 monoclonal antibody (mAb) on days 0 through 9 after grafting. Twelve to 14 days later, host cells infiltrating the HC-SMA were assessed for the development of allospe- Adhesion molecules intercellular adhesion molecule-1 (ICAM-1) and vascular cell adhesion molecule-1 (VCAM-1) are expressed on endothelial and some parenchymal cells. These adhesion molecules (ICAM-1 and VCAM-1) also appear to play important roles in vascularized organ allograft rejection, because antibodies directed against ICAM-1 and VCAM-1 have been shown to be effective in prolonging survival of vascularized murine cardiac allografts, cynomolgous monkey renal transplants, and human renal transplants, [1][2][3][4][5][6] as well as nonvascularized skin allografts. 7 ICAM-1 has been implicated in liver transplant rejection by studies that show increased levels of soluble ICAM-1 during rejection episodes and histological detection of increased ICAM-1 during liver allograft rejection. [8][9][10] Parenchymal cells may constitutively express or may be induced to express adhesion molecules by various cytokines. However, the role of adhesion molecules in the presentation of major histocompatibility complex (MHC) antigens by parenchymal cells is not known. Cytokines, including interleukin-1, interferon gamma, and tumor necrosis factor (TNF), have been shown to up-regulate hepatocyte expression of ICAM-1 and their adhesion to T lymphocytes in vitro. 11 However, the in vivo effects of various cytokines on adhesion molecule expression in the liver has not been described, and the consequences of in vivo cytokine exposure upon the immunogenicity of liver cells has not been reported.Previously, we demonstrated that purified hepatocytes in the absence of donor-type antigen-presenting cells are immunogenic in vitro in mixed lymphocyte hepatocyte culture as determined by their ability to stimulate proliferation and the development of allospecific cytolytic effector T cells (alloCTLs) in mixed lymphocyte hepatocyte culture. The observed immunogenicity was correlated with the expression of MHC class I antigens. 12 We have further demonstrated that purified hepatocytes are immunogenic in vivo and stimulate the development of allo-CTLs in sponge matrix allografts (SMA) bearing allogeneic hepatocytes. 13,14 In this report, we extend our previous in vivo studies using the hepatocytesponge matrix allograft (HC-SMA) model to examine the role of ICA...

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Immunohistochemical Study of Adhesion Molecules in Liver Inflammation

Cited by 200 publications

References 52 publications

Skeletal muscle cells: from local inflammatory response to active immunity

Skeletal muscle cells: from local inflammatory response to active immunity

Circulating intercellular adhesion molecule-1 (ICAM-1) in autoimmune liver disease and evidence for the production of ICAM-1 by cytokine-stimulated human hepatocytes

Efficacy of anti-intercellular adhesion molecule-1 immunotherapy on immune responses to allogeneic hepatocytes in mice

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