The authors of the original article “Taenia solium and Taenia crassiceps: miRNomes of the larvae and effects of miR-10-5p and let-7-5p on murine peritoneal macrophages” (Biosci Rep (2019) 39(11) BSR20190152), have realised that a splice had been introduced in Figure 7A of their article during their figure preparation. The original files used to create this figure have been assessed and approved by the Deputy Editor-in-Chief and the Editorial Board, and a version without this splice is presented below. The authors would also like to correct some typos in Table 3 of their article. The correct version of their table is also present in this Correction.

Effect of miR-10-5p (miR10) or let-7-5p (let7) on native or activated peritoneal macrophages

Figure 7
Effect of miR-10-5p (miR10) or let-7-5p (let7) on native or activated peritoneal macrophages

(A) Representative Ethidium Bromide-stained gel showing the RT-PCR-amplified fragments from the Gapdh, Nos2, Il6, Tgfb1, and Il1b genes. For RT-PCR, total RNA was extracted from the culture of naive peritoneal macrophages M(N) and activated with IFNγ M(IFNγ) or with IL-4 M(IL-4), which were not treated (-) or treated with miR10 or let7. (B) Bars represent the mean ± SEM of the expression level of target genes normalized to that of Gapdh, analyzed with Kodak Digital Science 1D Image Analysis software. The data are representative of three independent experiments (n = 3). *P<0.05; **P<0.01; ***P<0.001; ****P<0.0001, according to one-way ANOVA and Tukey's multiple comparisons test.

Figure 7
Effect of miR-10-5p (miR10) or let-7-5p (let7) on native or activated peritoneal macrophages

(A) Representative Ethidium Bromide-stained gel showing the RT-PCR-amplified fragments from the Gapdh, Nos2, Il6, Tgfb1, and Il1b genes. For RT-PCR, total RNA was extracted from the culture of naive peritoneal macrophages M(N) and activated with IFNγ M(IFNγ) or with IL-4 M(IL-4), which were not treated (-) or treated with miR10 or let7. (B) Bars represent the mean ± SEM of the expression level of target genes normalized to that of Gapdh, analyzed with Kodak Digital Science 1D Image Analysis software. The data are representative of three independent experiments (n = 3). *P<0.05; **P<0.01; ***P<0.001; ****P<0.0001, according to one-way ANOVA and Tukey's multiple comparisons test.

Table 3
Prediction of the putative immunologic gene targets of the most abundant T. solium and T. crassiceps miRs and their associated functions
miRNATargetmiR-function associated
miR-10-5p Ncor2, Bcl6, Il12/Il23p40 Promote the Treg production, negative regulator of Th1 and Th17 T cell differentiation. 
let-7-5p Il10, Il13, Ccr7 Promotes development of Th1, Th17 cells and IFN-γ ‐producing NKT cells. 
bantam-3p Mmd2, Tgfbr1 Regulation of cell proliferation. 
miR-125-5p Tnf, Irf4 Down- regulates pro-inflammatory signaling, promotes macrophage activation. Involved in WNT1 and TGF-β signaling, block the TNF biosynthesis 
miR-9a-5p Nfkb1, Mapk4 Negative regulator of TLR4 signaling 
mir-001-3p Cd69, Socs5, Traf3 Putative involved in T cell regulation 
mir-002-3p Slamf1, Vsir Putative involved in regulation of T cell cytokine production 
miRNATargetmiR-function associated
miR-10-5p Ncor2, Bcl6, Il12/Il23p40 Promote the Treg production, negative regulator of Th1 and Th17 T cell differentiation. 
let-7-5p Il10, Il13, Ccr7 Promotes development of Th1, Th17 cells and IFN-γ ‐producing NKT cells. 
bantam-3p Mmd2, Tgfbr1 Regulation of cell proliferation. 
miR-125-5p Tnf, Irf4 Down- regulates pro-inflammatory signaling, promotes macrophage activation. Involved in WNT1 and TGF-β signaling, block the TNF biosynthesis 
miR-9a-5p Nfkb1, Mapk4 Negative regulator of TLR4 signaling 
mir-001-3p Cd69, Socs5, Traf3 Putative involved in T cell regulation 
mir-002-3p Slamf1, Vsir Putative involved in regulation of T cell cytokine production 

The authors declare that these modifications do not affect the conclusions of their study.

This is an open access article published by Portland Press Limited on behalf of the Biochemical Society and distributed under the Creative Commons Attribution License 4.0 (CC BY).