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1

Lymphocytes distribution and intrahepatic compartmentalization during HCV infection: a main role of MHC-unrestricted T cells

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Agrati C., Nisii C., Oliva A., D?Offizi G., Montesano C., Pucillo L. P., Poccia F.
Archivum Immunologiae et Therapiae Experimentalis
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2002
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vol. 50
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issue 5
307-316
EN
Hepatitis-C virus (HCV) infection induces an acute and chronic liver inflammation through an immune mediated pathway that may lead to cirrhosis and liver failure. Indeed, HCV-related hepatitis is characterized by a dramatic lymphocyte infiltrate in the liver which is mainly composed by HCV non-specific cells. Several data indicated that IFN-gamma secretion by intrahepatic lymphocytes (IHL) may drive non specific cell homing to the liver inducing IP-10 production. An interesting hallmark of these IHL is the recruitment of lymphocytes associated with mechanism of innate immunity such as NK, NKT and gamma delta T lymphocytes. CD81 triggering on NK cell surface by the HCV envelope glycoprotein E2 was recently shown to inhibit NK cell function in the liver of HCV-infected persons resulting in a possible mechanism contributing to the lack of virus clearance and to the establishment of chronic infection. In contrast, intrahepatic NKT cells restricted to Cd1d molecules expressed on the hepatocyte surface may contribute to a large extent to the liver damage. Finally, an increased frequency of T cell expressing the gamma delta TCR was observed in HCV-infected liver and recent observations indicate that intrahepatic gamma delta T cell activation could be directly induced by the HCV/E2 particle through CD81 triggering. These cells are not HCV specific, are able to kill target cells including primary hepatocytes and their ability to produce Th1 cytokines is associated with an higher degree of liver disease. Altogether, CD1d/NKT and/or E2/CD81 interactions may play a major role in the establishment of HCV immunopathogenesis. In absence of virus clearance, the chemokine-driven recruitment of lymphocytes with an innate cytotoxic behavior in the liver of HCV infected patients may boost itself leading to the necroinflammatory and fibrotic liver disease.
2

Reactive oxygen intermediates and serum antioxidative system in patients with chronic C hepatitis treated with IFN-alpha and thymus factor X

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Jablonowska E., Tchorzewski H., Lewkowicz P., Kuydowicz J.
Archivum Immunologiae et Therapiae Experimentalis
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2005
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vol. 53
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issue 6
529-533
EN
In this study, the chemiluminescence (CL) of peripheral blood polymorphonuclear leukocytes (PMNLs) and the serum total antioxidative system (TAS) were assessed in patients with chronic C hepatitis (CCH) before and after 3 and 6 months of treatment with interferon (IFN)- and thymus factor X (TFX). The study included 26 patients with CCH aged between 25?63 years (mean: 42.67). Combined therapy with IFN-alpha 2a and a TFX preparation was applied. PMNL metabolic activity was assessed applying the whole-blood CL method. We measured CL response of neutrophils unstimulated and stimulated by opsonized zymosan, N-formyl-methionyl-leucyl-phenylalanine (N-fMLP), and phorbol-myristate-acetate (PMA) without and after priming with tumor necrosis factor alpha (10 ng/ml). The assessment of serum TAS was performed directly before the beginning of therapy with IFN-alpha and TFX and after 3 and 6 months of the treatment. A colorimetric method based on the reduction of the cationic radical ABTS+ (cation 2, 2'-azido-bis-[3-ethylobenzothiazolino-6-sulfonate]) in the presence of serum antioxidants was used. As a result of the treatment with IFN-alpha and TFX, the formation of free oxygen radicals by resting (unprimed) neutrophils increased statistically significantly both without stimulation and following stimulation by fMLP and PMA. A statistically significant increase in the serum antioxidant capacity was observed, which suggests the induction of compensatory processes. Increased in vitro reactive oxygen species production by both stimulated and unstimulated peripheral blood neutrophils of patients with CCH was observed. Treatment with IFN-alpha and TFX resulted in a compensatory increase in serum antioxidative capacity.
3

Immunology of viral co-infections with HIV

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Northfield J. W., Harcourt G., Lucas M., Klenerman P.
Archivum Immunologiae et Therapiae Experimentalis
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2005
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vol. 53
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issue 1
3-12
EN
Increasing clinical evidence is emerging that other persistent viral infections can act as important co-factors affecting the progression of human immunodeficiency virus-1 (HIV-1). It appears that hepatitis C (HCV) and cytomegalovirus (CMV) have a deleterious effect on HIV progression, whereas hepatitis G (GBV-C) benefits HIV-1 progression. At the same time, the aggressive nature of HCV infection in HIV is clearly recognized. Here we discuss this clinical evidence and go on to review scientific work pertaining to these interactions in the context of the known and theoretical immunological effects of these viruses. This is discussed at the level of the generation of adaptive immune responses and their effector functions. It is clear that co-infection with persistent viral infections may pose special problems for the human immune system, as pathogenic effects may not be specific to the actual eliciting virus and can therefore multiply the difficulties faced by host defenses. We also highlight the need for further therapies for HIV/HCV co-infected persons, as this is currently a complex and severe syndrome.
4

Pathogenesis and clinical consequences of iron overload in chronic hepatitis C- impact of host and viral factors related to iron metabolism

100%
Sikorska K., Romanowski T., Bielawski K. P.
Biotechnologia
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2011
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issue 1
54-65
EN
Chronic hepatitis C virus infection is a leading cause of progressive liver fibrosis, liver cirrhosis and hepatocellular carcinoma. Iron overload is frequently observed in cases of chronic hepatitis C and has been suggested as a negative prognostic factor for this disease. Although the mechanisms leading to iron accumulation are not fully explained yet, both host and viral factors seem to contribute towards the development of this pathology. Better understanding of the interplay between hepatitis C virus replication and expression of iron regulatory molecules may elucidate new and interesting targets for the effective treatment of chronic hepatitis C.
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