Analysis of cytokine production regulatory mechanism in basophils by immunoglobulin-like receptor PIR-B.

为了研究抑制型小鼠配对免疫球蛋白样受体PIR-B在调节嗜碱性粒细胞中th2型细胞因子产生中的潜在作用，我们使用逆转录病毒基因转移系统分析了PIR-B缺陷小鼠骨髓源性嗜碱性粒细胞。结果，我们发现PIR-B调节il -3诱导的小鼠嗜碱性细胞中IL-4的产生。此外，从使用各种PIR-B突变体的分析结果来看，在嗜碱性细胞上表达的PIR-B以不依赖于itim的方式负向调节il -3诱导的IL-4的产生，这表明PIR-B的调控机制以前未被认识到。

To examine the potential involvement of PIR-B, the inhibitory type murine paired immunoglobulin-like receptor, in the regulation of Th2-type cytokine production in basophils, we used retroviral gene transfer system and analyzed PIR-B-deficient mice bone marrow-derived basophils. As a result, we found that PIR-B regulates IL-3-induced IL-4 production in murine basophils. Moreover, from the result of analysis that used various PIR-B mutants, PIR-B expressed on basophils negatively regulates IL-3-induced IL-4 production in an ITIM-independent manner, pointing to previously unrecognized regulatory mechanisms by PIR-B.