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• W40196360 endingPage "64" @default.
• W40196360 startingPage "43" @default.
• W40196360 abstract "Systemic lupus erythematosus (SLE) is a chronic inflammatory disease accompanied by dysfunction of T and B lymphocytes and autoantibody production. Independent lines of evidence have implicated environmental factors and genetic determinants of the host in the causation of lupus (1). Cognate T-B recognition may be necessary to produce specific autoantibodies. Helper T cells from patients with active lupus enhance production of autoantibodies, whereas T cells from patients with inactive disease and from normal patients do not (1). Polymorphisms of HLA molecules regulating antigen presentation (2) and complement deficiency states (3) have been identified as inherited factors influencing disease susceptibility. However, the discordance rate of SLE may be as high as 70% among monozygotic twins (2), suggesting a significant role for exogenous agents. Initially, findings of virion-like tubuloreticular structures in endothelial cells and lymphocytes as well as demonstration of elevated serum levels of type I interferon raised the possibility of a viral etiology in lupus (4). Retroviruses were implicated by detection of retroviral p30 Gag protein in renal glomeruli and serum reactivities toward p30 Gag antigen in patients with SLE (5). Indeed, many features of human retroviral infections caused by HTLV-I and HIV-1 resemble those of SLE, and viral proteins have profound effects on both antigen presentation and effector functions of the immune system. Dysregulation of programmed cell death (PCD) has been documented in HIV-infected (6) and lupus patients as well (7). Similar to SLE, anemia (8), leukopenia (9), thrombocytopenia (10), polymyositis (11), and vasculitis have been widely reported in patients with AIDS (12). Direct virus isolation and transmission attempts from tissues of SLE patients have not been successful (13). Nevertheless, it is possible that a (retro)virus, responsible for provoking an immune response crossreactive with self antigens, has been cleared from the host; hence, the absence of viral particles is not conclusive. An alternative retroviral etiology, i.e., activation of endogenous retroviral sequences (ERSs), was initially proposed by a study of the New Zealand mouse model of SLE (14). Endogenous retroviral envelope glycoprotein, gp70, was found in immune-complex deposits of autoimmune lupus-prone NZB/NZW mice (14). Abnormal expression of an ERS was noted in the thymus of lupus-prone mouse strains (15,16). More recently, expression and autoantigenicity of human ERS has been demonstrated in patients with SLE (17–21)." @default.
• W40196360 created "2016-06-24" @default.
• W40196360 creator A5025875593 @default.
• W40196360 creator A5052080448 @default.
• W40196360 date "1999-01-01" @default.
• W40196360 modified "2023-10-11" @default.
• W40196360 title "Molecular Mimicry, Altered Apoptosis, and Immunomodulation as Mechanisms of Viral Pathogenesis in Systemic Lupus Erythematosus" @default.
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