Published June 15, 2015 - More info
Multiple myeloma (MM) is an age-dependent hematological malignancy. Evaluation of immune interactions that drive MM relies on in vitro experiments that do not reflect the complex cellular stroma involved in MM pathogenesis. Here we used Vk*MYC transgenic mice, which spontaneously develop MM, and demonstrated that the immune system plays a critical role in the control of MM progression and the response to treatment. We monitored Vk*MYC mice that had been crossed with
Camille Guillerey, Lucas Ferrari de Andrade, Slavica Vuckovic, Kim Miles, Shin Foong Ngiow, Michelle C.R. Yong, Michele W.L. Teng, Marco Colonna, David S. Ritchie, Martha Chesi, P. Leif Bergsagel, Geoffrey R. Hill, Mark J. Smyth, Ludovic Martinet
Original citation: J Clin Invest. 2015;125(5):2077–2089. doi:10.1172/JCI77181.
Citation for this corrigendum: J Clin Invest. 2015;125(7):2904. doi:10.1172/JCI82646.
The name of one of the authors, Marta Chesi, was incorrect. The correct author list is above.
The legend for Figure 3 did not indicate that the data on the survival of control WT mice reported in Figure 2E were duplicated in Figure 3F. The correct sentence is below.
The WT controls presented in Figure 3F are also presented in Figure 2E. All of the samples in these panels were derived from the same set of experiments.
The authors have also added Supplemental Figure 8 to clearly illustrate that the survival data in these panels were collected contemporaneously and that the statistical analyses accounted for multiple comparisons appropriately.
In addition, the legend for Figure 6 did not indicate that the data in Figure 6D on the mean γ-globulin percentages in the serum were also presented in Figure 5B. Further, the data in Figure 5D reporting the number of malignant CD138+CD155+ PCs in the BM of WT mice following cIg were also presented in Figure 6, E and H. The number of malignant CD138+CD155+ PCs in the BM of WT mice following α-CD137 treatment that are shown in Figure 6E are also reported in Figure 6H. The correct sentences are below.
The WT cIg samples displayed in Figure 6, D and E, are also presented in Figure 5, B and D, respectively. The WT cIg and WT α-CD137 samples in Figure 6E are also presented in Figure 6H. All of the samples in these panels were derived from the same set of experiments.
The authors have added Supplemental Figure 9 to clearly illustrate that the data for serum γ-globulin percentage and number of malignant CD138+CD155+ PCs were taken contemporaneously and that the statistical analyses accounted for multiple comparisons appropriately.
The authors also inadvertently presented the wrong FACS plot in Figure 7F for CD8+ T cells expressing CD69 following α-CD137 treatment. A label in Figure 7G has been corrected to indicate PBS treatment rather than cIg treatment. Typographical errors in Figure 7H have been corrected to indicate mice treated with α-CD137 + α-CD4 in Figure 7H. The correct panels are shown below.
Finally, the authors inadvertently presented the wrong panel of CTLA-4+ cells in Supplemental Figure 7B. In addition, the legend for Supplemental Figure 5C did not indicate that the vehicle groups were also presented in Figure 6H and were derived from the same set of experiments. The online version of the supplemental data file has been updated to correct these issues.
The authors regret the errors.