CONFLICT OF INTEREST Pancreatic involvement in murine antibody-mediated transfusion-related acute lung injury?

−29G>C polymorphism status in 28 weak D and 5 DEL patients of Korean ethnicity. As a result, we found that the RHD:c.149−29G>C variant was present in all samples with the R1 haplotype regardless of their D status (Table 1), confirming the linkage of this variant to the R1 haplotype. This finding is consistent with that of a recent study in which the RHD:c.149−29G>C variant was observed only in blood donors with a specific Rh haplotype (R1, R0, or Rz) regardless of their D status. 5 With this haplotype linkage information, we were able to determine RHD zygosity in three weak D samples with a CcEe phenotype (G/C: R1R2; C: R1r") (Table 1). Intronic variants outside the canonical splice sites may cause aberrant splicing, but the effect of these variants on the splicing process should be verified through functional studies. However, to date, no functional studies have been carried out to investigate the splicing effect of intronic variants distant from the canonical splice sites of the RHD gene, such as RHD:c.149−29G>C and RHD: c.802−38_35del. In fact, functional studies are costly and time consuming, rendering their use impractical in the clinical setting. As an alternative, a number of in silico tools for splicing defect prediction have been developed. We evaluated the potential impact of the RHD:c.149 −29G>C variant on splicing with the splicing prediction module of Alamut Visual version 2.15 (Interactive Biosoftware, Rouen, France). None of the four in silico tools incorporated in the software (SpliceSiteFinder-like, MaxEntScan, NNSPLICE, and GeneSplicer) predicted this variant to be deleterious. In conclusion, RHD:c.149−29G>C listed as RHD* 01EL.32 is a benign intronic variant linked to the R1, R0, and Rz haplotypes, and this allele should be removed from the ISBT allele table as a cause of a DEL phenotype. Also, one should be cautious about concluding, without well-established functional studies, that intronic variants outside the canonical splice sites affect D antigen expression. CONFLICT OF INTEREST The authors declare no conflicts of interest.