Knockdown of SF2/ASF decreased expression of full-length CD200 in both Daudi and SK-N cells. Consistent with data seen following mutation or deletion of the ESE, the expression pattern of CD200 was again reversed in SK-N cells. The western blot performed confirmed the efficiency of knockdown of SF2/ASF. In contrast, overexpression of SF2/ASF increased expression of full-length CD200 but only in the presence of the ESE in exon 2, highlighting the critical role of the ESE in the mechanism of alternative splicing of CD200. Ubiquitously expressed splicing factors, among them is SF2/ASF, are thought to control tissue specific alternative splicing through their different expression levels in different tissues (44) . Our result showed that the natural level of SF2/ASF was higher in the neuronal cell line SK-N than in B cell line Daudi. This may help explain why endogenous full-length CD200 (exon 2 inclusion) is expressed at much higher level than that of truncated CD200 (exon 2 exclusion) in SK-N.