FCERI mediated NF-kB activation

The increase in intracellular Ca+2 in conjunction with DAG also activates PKC and RasGRP, which inturn contributes to cytokine production by mast cells (Kambayashi et al. 2007). Activation of the FCERI engages CARMA1, BCL10 and MALT1 complex to activate NF-kB through PKC-theta (Klemm et al. 2006, Chen et al. 2007). FCERI stimulation leads to phosphorylation, and degradation of IkB which allows the release and nuclear translocation of the NF-kB proteins. Activation of the NF-kB transcription factors then results in the synthesis of several cytokines. NF-kB activation by FCERI is critical for proinflammatory cytokine production during mast cell activation and is crucial for allergic inflammatory diseases (Klemm et al. 2006).

细胞内钙离子（Ca+2）的升高与二酰基甘油（DAG）的共存激活蛋白激酶C（PKC）和RasGRP，进而促进肥大细胞的细胞因子生成（Kambayashi 等人，2007年）。免疫球蛋白E受体（FCERI）的激活引发CARMA1、BCL10和MALT1复合物的形成，进而通过PKC-theta激活核因子κB（NF-kB）（Klemm 等人，2006年，Chen 等人，2007年）。FCERI的刺激导致IkB的磷酸化和降解，从而允许NF-kB蛋白的释放和向细胞核的转位。随后，NF-kB转录因子的激活导致多种细胞因子的合成。FCERI通过激活NF-kB在肥大细胞活化过程中促进促炎细胞因子的生成，这对于过敏性炎症疾病至关重要（Klemm 等人，2006年）。