Anti-Fcer1a Monoclonal antibody, clone NBS-2 [FITC]

Immunoglobulin E (IgE) activates mast cells (MCs). It remains unknown whether IgE also activates other inflammatory cells, and contributes to the pathogenesis of abdominal aortic aneurysms (AAAs). This study demonstrates that CD4(+) T cells express IgE receptor FceR1, at much higher levels than do CD8(+) T cells. IgE induces CD4(+) T-cell production of IL6 and IFN-gamma, but reduces their production of IL10. Fc epsilon R1 deficiency (Fcer1a(-/-)) protects apolipoprotein E-deficient (Apoe(-/-)) mice from angiotensin-II infusion-induced AAAs and reduces plasma IL6 levels. Adoptive transfer of CD4(+) T cells (but not CD8(+) T cells), MCs, and macrophages from Apoe(-/-) mice, but not those from Apoe(-/-) Fcer1a(-/-) mice, increases AAA size and plasma IL6 in Apoe(-/-) Fcer1a(-/-) recipient mice. Biweekly intravenous administration of an anti-IgE monoclonal antibody ablated plasma IgE and reduced AAAs in Apoe(-/-) mice. Patients with AAAs had significantly higher plasma IgE levels than those without AAAs. This study establishes an important role of IgE in AAA pathogenesis by activating CD4(+) T cells, MCs, and macrophages and supports consideration of neutralizing plasma IgE in the therapeutics of human AAAs.

Background: Immunoglobulin E (IgE) is a central player in the allergic response, and raised total IgE levels are considered as an indicator of atopy or potential development of atopy. A recent genome-wide scan in a German population-based cohort of adults identified the gene encoding the alpha chain of the high affinity receptor for IgE (FCER1A) as a susceptibility locus influencing total serum IgE levels. The aim of this study was to investigate whether the polymorphisms in the FCER1A gene are associated with allergic rhinitis (AR) in a Han Chinese population. Methodology/Principal Findings: A population of 378 patients with AR and 288 healthy controls was studied. Precise phenotyping of patients was accomplished by means of a questionnaire and clinical examination. Blood was drawn for DNA extraction and total serum immunoglobulin E (IgE) measurement. A total of 16 single nucleotide polymorphisms (SNPs) in FCER1A were selected and individually genotyped. None of the SNPs in the FCER1A showed an association with AR. Similarly, the lack of association was also evident in subgroup analysis for the presence of different allergen sensitivities. None of the selected SNPs in FCER1A was associated with total IgE level. Conclusions: Although FCER1A presents itself as a good candidate for contributing to total serum IgE, this study failed to find an association between SNPs in the FCER1A gene region and IgE level or AR susceptibility.