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Hannah M Cheeseman, Ann M Carias, Abbey B Evans, Natalia J Olejniczak, Paul Ziprin, Deborah F L King, Thomas J Hope, Robin J Shattock
The majority of new Human Immunodeficiency Virus (HIV)-1 infections are acquired via sexual transmission at mucosal surfaces. Partial efficacy (31.2%) of the Thai RV144 HIV-1 vaccine trial has been correlated with Antibody-dependent Cellular Cytotoxicity (ADCC) mediated by non-neutralizing antibodies targeting the V1V2 region of the HIV-1 envelope. This has led to speculation that ADCC and other antibody-dependent cellular effector functions might provide an important defense against mucosal acquisition of HIV-1 infection...
2016: PloS One
Rafael N Moresco, Marijn M Speeckaert, Slawomir C Zmonarski, Magdalena Krajewska, Ewa Komuda-Leszek, Agnieszka Perkowska-Ptasinska, Loreto Gesualdo, Maria T Rocchetti, Sigurd E Delanghe, Raymond Vanholder, Wim Van Biesen, Joris R Delanghe
BACKGROUND: IgA nephropathy (IgAN) and Henoch-Schönlein purpura nephritis (HSPN) are glomerular diseases that share a common and central pathogenic mechanism. The formation of immune complexes containing IgA1, myeloid IgA Fc alpha receptor (FcαRI/CD89) and transglutaminase-2 (TG2) is observed in both conditions. Therefore, urinary CD89 and TG2 could be potential biomarkers to identify active IgAN/HSPN. METHODS: In this multicenter study, 160 patients with IgAN or HSPN were enrolled...
June 2016: BBA Clinical
Sebastian M Lechner, Lilia Abbad, Erwan Boedec, Christina Papista, Marie-Bénédicte Le Stang, Christelle Moal, Julien Maillard, Agnès Jamin, Julie Bex-Coudrat, Yong Wang, Aiqun Li, Paolo G V Martini, Renato C Monteiro, Laureline Berthelot
IgA nephropathy (IgAN), characterized by mesangial IgA1 deposits, is a leading cause of renal failure worldwide. IgAN pathogenesis involves circulating hypogalactosylated IgA1 complexed with soluble IgA Fc receptor I (sCD89) and/or anti-hypogalactosylated-IgA1 autoantibodies, but no specific treatment is available for IgAN. The absence of IgA1 and CD89 homologs in the mouse has precluded in vivo proof-of-concept studies of specific therapies targeting IgA1. However, the α1KI‑CD89Tg mouse model of IgAN, which expresses human IgA1 and human CD89, allows in vivo testing of recombinant IgA1 protease (IgA1‑P), a bacterial protein that selectively cleaves human IgA1...
September 2016: Journal of the American Society of Nephrology: JASN
Thomas Robert, Laureline Berthelot, Alexandra Cambier, Eric Rondeau, Renato C Monteiro
Immunoglobulin IgA nephropathy (IgAN) is the leading form of primary glomerulonephritis associated with end-stage renal failure, requiring either dialysis or renal transplantation. Microscopic hematuria and proteinuria are the most common presentations, and mesangial cell proliferation with IgA deposition are found in renal biopsies. There is growing evidence that IgAN is an immune complex (IC)-mediated disease. To date, three key molecules have been implicated in IC formation, correlating with disease progression/recurrence after transplantation: galactose-deficient IgA1 (Gd-IgA1), IgG anti-Gd-IgA1 antibodies, and soluble CD89 (an Fc receptor for IgA)...
December 2015: Trends in Molecular Medicine
Sebastian M Lechner, Christina Papista, Jonathan M Chemouny, Laureline Berthelot, Renato C Monteiro
Immunoglobulin A nephropathy (IgAN) or Berger's disease is the most common form of primary glomerulonephritis in the world and one of the first causes of end-stage renal failure. IgAN is characterized by the accumulation of immune complexes containing polymeric IgA1 in mesangial areas. The pathogenesis of this disease involves the deposition of polymeric and hypogalactosylated IgA1 (Gd-IgA1) in the mesangium. Quantitative and structural changes of Gd-IgA1 play a key role in the development of the disease due to functional abnormalities of two IgA receptors: the FcαRI (CD89) expressed by blood myeloid cells and the transferrin receptor (CD71) on mesangial cells...
February 2016: Journal of Nephrology
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