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

为了研究抑制性小鼠成对免疫球蛋白样受体PIR-B对嗜碱性粒细胞Th2型细胞因子产生的调节作用，我们利用逆转录病毒基因转移系统分析了PIR-B缺陷小鼠骨髓来源的嗜碱性粒细胞。结果，我们发现PIR-B调节IL-3诱导的小鼠嗜碱性粒细胞产生IL-4。此外，从使用各种PIR-B突变体的分析结果来看，表达在嗜碱性细胞上的PIR-B以不依赖ITIM的方式负面调节IL-3诱导的IL-4的产生，表明PIR-B以前未发现的调节机制。

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.