Báo cáo y học: "Coaggregation of Fc RI with Fc RIIB Inhibits Degranulation but Not Induction of Bcl-2 Family Members A1 and Bim in Mast Cells"

Tuyển tập các báo cáo nghiên cứu về y học được đăng trên tạp chí y học General Psychiatry cung cấp cho các bạn kiến thức về ngành y đề tài: Coaggregation of Fc RI with Fc RIIB Inhibits Degranulation but Not Induction of Bcl-2 Family Members A1 and Bim in Mast Cells. | Original Article Coaggregation of FceRI with FcyRIIB Inhibits Degranulation but Not Induction of Bcl-2 Family Members A1 and Bim in Mast Cells Maria Ekoff MSc Christine Moller PhD Zou Xiang PhD Gunnar Nilsson PhD Abstract The aggregation of high-affinity immunoglobulin E IgE receptors FceRI on mast cells is a critical event in the initiation of an allergic reaction. Coengagement of FceRI with immunoglobulin G IgG low-affinity receptor Fc RIIB CD32 inhibits degranulation and the release of inflammatory mediators from mast cells and has therefore been proposed as a new therapeutic approach for the treatment of allergies. In this study we investigated whether Fc RIIB besides inhibiting degranulation negatively regulates other signalling pathways downstream of FceRI. For this we determined the phosphorylation and or expression of proteins involved in the regulation of mast-cell apoptosis. Coaggregation led to an attenuation of Akt phosphorylation but did not inhibit phosphorylation of transcription factor Foxo3a or its proapoptotic target Bim. Similarly FceRI-dependent expression of the prosurvival gene A1 was not affected by coaggregation. Our data demonstrate that coengagement of FceRI and Fc RIIB inhibits degranulation but not the signalling pathways regulating Bcl-2 family members Bim and A1. Mast cells are critical effector cells mediating immunoglobulin E IgE -dependent allergic responses. Binding of an allergen to IgE already bound to its high-affinity receptor FceRI on mast cells leads to aggregation and subsequent activation. This initiates signalling events that typically result in degranulation changes in gene expression and the release of inflammatory mediators contributing to acute and late-phase allergic M. Ekoff C. Moller G. Nilsson Department of Medicine Clinical Immunology and Allergy Unit Karolinska Institutet Stockholm Sweden Z. Xiang Cambridge Institute for Medical Research Cambridge United Kingdom Correspondence to Dr. Gunnar Nilsson Karolinska .

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