On page 2416 in the 19 November 2015 issue, under “Gene expression analysis,” the text cites reference 27 by Liang et al1  as a source of incorrect primer sequences used to measure transcript levels of Peli1, Irf8, Malt1, and Ccl22 in Figures 3 to 5. The correct primer sequences are listed in revised supplemental Table 3 of Liang et al1  as irf8-a, peli1-a, malt1-a, and ccl22-a (see the accompanying erratum2 ).

The data shown in Figures 3 to 5 were generated with gene-specific primers of a different sequence, designated primer set “a” in revised supplemental Table 3 of Liang et al.1  The primers for Irf8, Malt1, Ccl22, and Peli1 listed in the original supplemental Table 3 are designated primer set “b” in the revised supplemental Table 3.1  Primers irf8-a and ccl22-a amplify a region within the 3′ untranslated region of Irf8 and Ccl22 RNA, respectively. Primers malt1-a and peli1-a amplify regions in partially processed transcripts denoted in the National Center for Biotechnology Information gene repository as “retained introns.” Primers denoted “b” for these 4 genes amplify fragments of spliced transcripts only, with forward and reverse primers binding to separate exons. Although primer sets “a” and “b” yield comparable results for the abundance of Irf8, Ccl22, Malt1, and Peli1 transcripts in cultured RAW cells and mouse tissues, data generated with primer set “a” cannot be interpreted to indicate the prevalence of fully processed messenger RNA (mRNA) or the abundance of protein product translated from such mRNAs and hence should be considered biomarkers only.

The authors apologize for these errors.

1.
Liang
HPH
,
Kerschen
EJ
,
Hernandez
I
, et al
.
EPCR-dependent PAR2 activation by the blood coagulation initiation complex regulates LPS-triggered interferon responses in mice
.
Blood
.
2015
;
125
(
18
):
2845
-
2854
.
2.
Erratum for Liang HPH
,
Kerschen
EJ
,
Hernandez
I
, et al
.
EPCR-dependent PAR2 activation by the blood coagulation initiation complex regulates LPS-triggered interferon responses in mice
.
Blood
.
2018
;
131
(
22
):
2508
.
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