Anti-FCAR monoclonal antibody, clone MIP8a [R-PE]

Here, we compare the architecture of membrane receptors with extracellular lg-like domains located within the leukocyte lg-like receptor complex (LRC) of humans and mice. The receptors can be classified broadly into four groups, based on the homology of their lg-like domains and gene architecture. Receptors in the first group are characterized by the presence of the lg constant type 2-1 (lgC2-1) and variant lg (vlg) domains, and include the leukocyte lg-like receptors (LlLRs) and murine paired lg-activating receptors (PlRs). The second group of receptors possess an lgC2-2 domain and comprise the killer-cell lg-like receptors (KlRs) and platelet collagen receptor glycoprotein Vl (GPVI). The third group consists of receptors with lgC2-1, and lgC2-3 or lgC2-4 domains, and includes the receptor for lgA Fc (FCAR), NKp46 and murine Ly94. The fourth group with a single extracellular lgC2-1 domain, consists of the leukocyte-associated lg-like receptors (LAlRs). The genomic organization of and evolutionary associations between these receptors and their domains are examined.

IgA nephropathy is characterized by a high heterogeneity of clinical expression with 10-30% of patients progressing to end-stage renal failure. The gene of the Fc alpha RI or CD89 presents a single-nucleotide polymorphism responsible for a proinflammatory phenotype of neutrophils in vitro and ex vivo. The aim of our study was to assess whether this CD89 polymorphism 844 A-> G is (i) a marker of disease susceptibility and/or (ii) associated with a more severe prognosis. All patients diagnosed with IgA nephropathy and for whom DNA frozen sample was available were included in this European monocentric retrospective analysis and compared to a cohort of healthy volunteers. Allelic discrimination was performed by real-time quantitative polymerase chain reaction (Applied Biosystems (TM)). We first compared the distribution of A and G alleles between patients and volunteers and then studied the relationships between alleles and renal survival, histological score, proteinuria and renal function at diagnosis. Seven hundred and twenty-six patients were analyzed for the study of susceptibility and 425 in the association study. The presence of the G allele was not associated with the occurrence of IgA nephropathy (chi(2) test 0.57, ns). Likewise, renal survival and the criteria for disease activity at time of diagnosis were not affected by the presence of the G allele. No significant association between 844 A-> G CD89 polymorphism and the expression of the IgA nephropathy in Caucasians exists. This result does, however, not preclude the implication of other CD89 polymorphisms neither the possibility for a role of CD89 in the pathogenesis of IgA nephropathy.