Browsing by Author "Soza, A."

Now showing 1 - 5 of 5
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    Autoantibodies against galectin-8: their specificity, association with lymphopenia in systemic lupus erythematosus and detection in rheumatoid arthritis and acute inflammation
    (SAGE PUBLICATIONS LTD, 2009) Massardo, L.; Metz, C.; Pardo, E.; Mezzano, V.; Babul, M.; Jarpa, E.; Guzman, A. M.; Andre, S.; Kaltner, H.; Gabius, H. J.; Jacobelli, S.; Gonzalez, A.; Soza, A.
    The role of autoantibodies in the pathogenesis of systemic lupus erythematosus (SLE) has not been completely defined. From more than a hundred autoantibodies described in SLE, relatively few have been associated with clinical manifestations. The glycan-binding proteins of the galectin family can modulate the immune system. Anti-galectin autoantibodies thus could have functional and/or pathogenic implications in inflammatory processes and autoimmunity. We previously reported function-blocking autoantibodies against galectin-8 (Gal-8) in SLE. Here we tested these autoantibodies against a series of other human galectins and demonstrated their specificity for Gal-8, being detectable in 23% of 78 SLE patients. Remarkably, they associated with lymphopenia (50% of 18 anti-Gal-8-positive versus 18% of 60 anti-Gal-8-negativecases, Fisher's Exact test two-tailed: P < 0.012). Lymphopenia is a common clinical manifestation in SLE, yet of unknown mechanism. In addition, six of eight patients with both lymphopenia and malar rash had anti-Gal-8 in their sera. Occurrence of these autoantibodies was not confined to SLE as we also found them in sera of patients with rheumatoid arthritis (16%) and septicemia (20%). This study thus establishes occurrence of specific anti-Gal-8 autoantibodies in autoimmune rheumatic diseases and in acute inflammation, with an apparent association to a clinical subset in SLE. Lupus (2009) 18, 539-546.
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    Autoimmune reactivity against the 20S-proteasome includes immunosubunits LMP2 (beta 1i), MECL1 (beta 2i) and LMP7 (beta 5i)
    (OXFORD UNIV PRESS, 2008) Scheffler, S.; Kuckelkorn, U.; Egerer, K.; Doerner, T.; Reiter, K.; Soza, A.; Burmester, G. R.; Feist, E.
    Objectives. Autoantibodies against the 20S-proteasome display a broad diversity with a remarkably low frequency of individual cross-reactivity against the different subunits of the proteasome. Although their pathogenic and diagnostic significance remains obscure, an involvement in the clearance of circulating proteasomes as well as an interaction with the activity of the proteolytic complex was assumed in previous studies.
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    Hepatitis C virus quasispecies in plasma and peripheral blood mononuclear cells of treatment naive chronically infected patients
    (WILEY, 2009) Vera Otarola, J.; Barria, M. I.; Leon, U.; Marsac, D.; Carvallo, P.; Soza, A.; Lopez Lastra, M.
    Peripheral blood mononuclear cells (PBMCs) from 45 treatment naive, HIV-negative, chronically hepatitis C virus (HCV)-infected patients were analyzed for the presence of HCV RNA. Viral RNA was detected in 73% of the studied patients. Single-strand conformation polymorphism assays and sequence analysis of the HCV 5'untranslated regions amplified from RNA recovered from both Plasma and PBMCs suggested virus compartmentalization in 57.6% of patients studied. In summary, our study presents evidence that HCV RNA can be found in PBMCs of treatment naive chronically infected patients that are not immunocompromised or co-infected with the human immunodeficiency virus.
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    Incidence and prevalence of hepatitis C virus infection in Chile.
    (2005) González, R.; Soza, A.; Hernández, V.; Pérez, R.M.; Alvarez, M.; Morales, A.; Arellano, M.; Riquelme, A.; Viviani, P.; Covarrubias, C.; Arrese, M.; Miquel, J.F.; Nervi, F.
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    Low- and standard-dose peginterferon alfa-2a for chronic hepatitis C, genotype 2 or 3: efficacy, tolerability, viral kinetics and cytokine response
    (WILEY-BLACKWELL PUBLISHING, INC, 2010) Rotman, Y.; Borg, B. B.; Soza, A.; Feld, J. J.; Modi, A. A.; Loomba, R.; Lutchman, G.; Rivera, E.; Doo, E.; Ghany, M. G.; Heller, T.; Neumann, A. U.; Liang, T. J.; Hoofnagle, J. H.
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