There were errors published in J. Cell Sci. 2011 124, 3029–3037.

The names of the following people were listed but should have been omitted from the list of authors:

Neil Phillips, Andrew Fire, Dolly Tyan, Mark Kay

Fig. 2 contains the following errors:

  • An incorrect image of panel was published.

  • Instead of eight, a total of ten animals made up both control groups that lead to the data shown in the graph.

  • An incorrect image of panel c has been published.

  • Balb/c cellular immune activation on the same day was significantly weaker after hESCKD rather than hESC transplantation. Spot frequencies of IFN-γ and IL-4 (P=0.001 and P<0.001, respectively) were significantly lower after hESCKD transplantation (d) when compared with hESCs.

The correct Fig. 2 is shown below.

Fig. 2.

Transplantation of hypoantigeneic hESC. (a) HLA I knockdown in hESCKD was followed by flow cytometry and showed levels between 1% and 12% of those of naïve hESC between days 7 and 42 (means ± s.e.m.). (b) A total of 106 hESCs or hESCKD were transplanted into the gastrocnemius muscle of either immunocompetent Balb/c or severely immunocompromised SCID-beige mice. All ten Balb/c mice rapidly rejected the hESC transplants, whereas the cells survived in ten SCID-beige recipients. Rejection of hESCKD was markedly attenuated and four out of ten hESCKD grafts achieved long-term survival. (c) On day 5, BLI signals from hESCs in SCID-beige and hESCKD in Balb/c were similarly strong, whereas signals from hESCs in Balb/c were negligible. (d) Balb/c cellular immune activation on the same day was significantly weaker after hESCKD rather than hESC transplantation with significantly lower IFN-γ (*P=0.001) and IL-4 spot frequencies (†P<0.001). (e) The percentage of Treg cells (CD25+ Foxp3+ cells) among the CD4+ population in inguinal lymph nodes was monitored over time. The Treg fraction increased after both hESC and hESCKD transplantation (*P<0.05 compared with native Balb/c) but remained elevated only in the hESCKD group (§P<0.05 compared with hESC after 14 days).

Fig. 2.

Transplantation of hypoantigeneic hESC. (a) HLA I knockdown in hESCKD was followed by flow cytometry and showed levels between 1% and 12% of those of naïve hESC between days 7 and 42 (means ± s.e.m.). (b) A total of 106 hESCs or hESCKD were transplanted into the gastrocnemius muscle of either immunocompetent Balb/c or severely immunocompromised SCID-beige mice. All ten Balb/c mice rapidly rejected the hESC transplants, whereas the cells survived in ten SCID-beige recipients. Rejection of hESCKD was markedly attenuated and four out of ten hESCKD grafts achieved long-term survival. (c) On day 5, BLI signals from hESCs in SCID-beige and hESCKD in Balb/c were similarly strong, whereas signals from hESCs in Balb/c were negligible. (d) Balb/c cellular immune activation on the same day was significantly weaker after hESCKD rather than hESC transplantation with significantly lower IFN-γ (*P=0.001) and IL-4 spot frequencies (†P<0.001). (e) The percentage of Treg cells (CD25+ Foxp3+ cells) among the CD4+ population in inguinal lymph nodes was monitored over time. The Treg fraction increased after both hESC and hESCKD transplantation (*P<0.05 compared with native Balb/c) but remained elevated only in the hESCKD group (§P<0.05 compared with hESC after 14 days).

Fig. 5 contains the following errors:

(a, b) After incubation with CD3+ CD56− lymphocytes, hESCs (P<0.001 and P=0.005) but not hESCKD (P=1.0 and P=0.708) significantly increased the spot frequencies for IFN-γ(a) and IL-4 (b), respectively, compared with resting responder lymphocytes.

The correct Fig. 5 is shown below.

Fig. 5.

Allogeneic cytotoxic killing of hESC. Human PBMCs were separated into lymphocytes (CD3+ CD56−) and NK cells (CD3− CD56+). IFN-γ(a) and IL-4 (b) Elispot assays revealed that only hESCs (†P<0.001 and *P=0.005), and not hESCKD (P=1.0 and P=0.708), significantly induced allogeneic lymphocyte activation in vitro compared with responder lymphocytes. NK cell activation (c) and CD107a surface expression (d) were provoked by either PMA plus ionomycin stimulation or K562 incubation. *P<0.05 and †P<0.001 compared with responder NK cells. Both hESCs and hESCKD did not induce significant NK cell activation.

Fig. 5.

Allogeneic cytotoxic killing of hESC. Human PBMCs were separated into lymphocytes (CD3+ CD56−) and NK cells (CD3− CD56+). IFN-γ(a) and IL-4 (b) Elispot assays revealed that only hESCs (†P<0.001 and *P=0.005), and not hESCKD (P=1.0 and P=0.708), significantly induced allogeneic lymphocyte activation in vitro compared with responder lymphocytes. NK cell activation (c) and CD107a surface expression (d) were provoked by either PMA plus ionomycin stimulation or K562 incubation. *P<0.05 and †P<0.001 compared with responder NK cells. Both hESCs and hESCKD did not induce significant NK cell activation.

The funding section has been accidentally omitted and should read:

S.S. received funding from the Deutsche Forschungsgemeinschaft (DFG; SCHR 992/3-1, SCHR 992/4-1).

In supplementary material Fig. S2, the BLI image of the hind limb (panel b) is incorrect. The published legend is correct.

The correct panel b is shown below.

The first author apologises for these errors.