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Squamous Cell Carcinoma Antigen (SCCA) expression and CD27+ memory B lymphocytes in patients with chronic hepatitis C
... A common mechanism for autoimmune response is a secondary necrosis of non-ingested apoptotic cells, favoring responses against themselves. The link between SLE and apoptotic cell clearance is emphasized by the fact that immunization with dendritic cells loaded with apoptotic cells can induce autoantibodies, but sustained disease only occurs in susceptible situations [40]. An increased production of apoptotic bodies with a strong reduction of serum DNase activity, which is involved in their clearance, has been detected in SLE patients. ...
... In SLE patients with nephrotic syndrome an increase of the SERPINB3 has been reported in serum, not related with SLE activity but ascribed to renal failure [39]. Recent data obtained in our laboratories indicate that SERPINB3 was expressed on the surface of B lymphocytes in the majority of normal subjects but in none of SLE patients [40]. Since a direct correlation of surface SERPINB3 with the memory B cell marker CD27 was documented, a possible involvement of SERPINB3 in B cell defects in SLE could be speculated. ...
SERPINB3 (Squamous Cell Carcinoma Antigen, SCCA1) is a member of the ov-serpins, a serine protease inhibitors family expressed in many cell types including normal epithelium, leukocytes, tumors of epithelial origin and primary liver cancer. Several studies, carried out in vitro and in vivo, have documented an important role of SERPINB3 in the modulation of programmed cell death by different mechanisms, both in inflammatory processes and in cancer. SERPINB3 significantly attenuates apoptosis by contrasting cytochrome c release from the mitochondria and by antichemotactic effect for NK cells. Mechanisms involved in apoptosis induction and regulation play a key role in the balance between cell proliferation and death. Imbalance of this equilibrium may contribute to the development of autoimmune diseases, as defective apoptosis of immune cells leads to deregulated autoreactive cell proliferation. Since defective programmed cell death represents a critical feature of autoimmunity, the involvement of SERPINB3 in this pathological field deserves further studies.
... Previous studies indicate that the serpin Squamous Cell Carcinoma Antigen (SCCA) is the major cellular protein involved in the binding of HBV to liver cell surface via the interaction with preS1 encoded surface protein of the virus [37]. Since recent findings indicate that B lymphocytes and, to a lesser extent, also monocytes express this serpin on their surface [38], it is likely that the virus entry into peripheral blood cells occurs using the same mechanisms already described for liver infection. ...
The liver is the main site of HBV replication, however extrahepatic organs, such as the lymphoid system, are an important reservoir of the virus. Viral DNA into different mononuclear cell subsets has been mainly detected in monocytes and B lymphocytes. The attachment site of the virus has been identified in the preS1 encoded protein of the virus envelope, the same involved in hepatocyte infection. The risk of HBV transmission by infected lymphocytes has been clearly documented in the setting of liver transplantation where de novo HBV infection has been found in up to about 80% of liver grafts from HBsAg negative but anti-HBc positive donors. In the hemodialysis setting the percentage of HBV DNA detection in mononuclear cells of HBsAg negative patients has been described in up to 54% of the cases. Vertical transmission studies indicate that HBV-infected mononuclear cells of the mother may result in viral infection of mononuclear cells of the newborns and possible HBV vaccine response failure. HBV can also infect bone marrow cells and in vitro studies demonstrate a block of hematopoiesis by HBV, supporting clinical observations of isolate cases of aplastic anemia associated to the infection.
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