已知tlr 2活化会促进抗原呈现细胞表面共同刺激分子的表现，但其调控机制及讯息传递路径仍不是非常清楚。
TLR2 is reported to enhance the expression of costimulatory molecules on the antigen presenting cell, however the regulatory mechanisms are still unclear.
我们偶然发现送入细胞内的STAT1C过量表现会造成LL2 细胞异常的STAT蛋白活化，进一步研究其机制也许能发现一些新的JAK/STAT讯息传递路径的调节系统。
We incidentally found that STAT1C overexpression cause aberrant STAT activation in LL2 cells. Further studies on the underlying mechanisms may explore a novel regulatory system of JAK/STAT pathway.
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