In the article entitled “Ectopic T-Cell Specificity and Absence of Perforin and Granzyme B Alleviate Neural Damage in Oligodendrocyte Mutant Mice,” (Volume 176, pages 549–555 of the February 2010 issue of The American Journal of Pathology), Figure 1B, page 552, contained an error. The images for T lymphocytes lacking TCR (OT-I) (middle image) and T lymphocytes lacking perforin (perforin−/−) (right image) were inadvertently duplicated, although arrows were differently placed. The authors assert that the correction of this mistake does not alter the conclusions of the article. The corrected Figure 1 (with legend) appears in adjacent column.
Figure 1.
Neural damage in PLPtg mice depends on an intact TCR repertoire and molecules typical for cytotoxic T-lymphocytes. A: Quantification of periaxonal vacuoles in semithin sections of optic nerves from PLPwt mice and PLPtg mutants with normal or molecularly altered T-lymphocytes. Note reduction in vacuole numbers when T-lymphocytes lack relevant TCR (OT-I) or the cytotoxic molecules perforin and Gzmb. B: Representative semithin sections from PLPtg mutants with wild-type immune system, with irrelevant TCR (OT-I) and with lymphocytes lacking perforin (perforin−/−). Note reduced vacuole numbers when T-lymphocytes lack relevant TCR (OT-I) or the cytotoxic molecule perforin. Arrows point to periaxonal vacuoles. Scale bar = 50 μm. C: Representative electron micrographs from optic nerves of PLPwt mice, PLPtg mutants with wild-type immune system (PLPtg/RAG-1−/− BMCwt), and of PLPtg mutants with irrelevant TCR (PLPtg/RAG-1−/− OT-I). Note normal appearance of myelin in the PLPwt mice (left) and occurrence of myelin vacuoles in PLPtg mutants with wild-type immune system (middle; asterisk). Remnant of an axon is indicated by a double asterisk. In PLPtg mutants with irrelevant TCR (right), demyelination and formation of vacuoles is substantially reduced. Occasionally, formation of redundant myelin loops (arrow) is seen. Scale bar = 1 μm. D: Reduction in MBP immunoreactivity in optic nerves from PLPtg mutants with normal or molecularly altered T-lymphocytes indicative of demyelination. Note that loss of MBP is minimized in the absence of relevant TCR or perforin, whereas absence of Gzmb apparently does not reduce demyelination. PLPwt mice do not show demyelination. *P < 0.05, **P ≤ 0.01, n = 3 to 6 per group.
In the article entitled, “Tracheal Basal Cells: A Facultative Progenitor Cell Pool” (Volume 177, pages 362–376 of the July 2010 issue), the legend to Figure 6, page 371, contained errors regarding which proteins were recognized via immunofluroescence staining. The legend should have appeared as below.
Figure 6. Basal cell response to naphthalene-mediated tracheal injury. A–J: Dual immunofluorescence analysis of CCSP (red) and basal cell keratins in the intercartilagenous (keratin 5; green) (A, C, E, G, I) and midcartilagenous (keratin 14; green) (B, D, F, H, J) regions. Arrows in E and F indicate cells that expressed only keratin 14. K: mRNA abundance as a function of time after injury. Note log scale in K. Keratin (K) 5, 15, and 14. Mean ± SEM, n = 4. All keratin 14 values are significantly different from day 0, P < 0.0005. All keratin 5 and 15 values are significantly different from day 0, P < 0.05. L: Morphometric analysis of keratin 5+ (red) and keratin 14+ (blue) cell distribution as a function of position along the proximal to distal axis of the ventral trachea. Analysis of four mice is shown. M–N: Stereological methods were used to determine the mass of keratin 5+ cells (M) and keratin 14+ cells (N) in the intercartilaginous (ICR) and midcartilaginous (MCR) regions of the control (white bars) and naphthalene recovery day 6 trachea (black bar). Mean ± SD, n = 4. The mass of keratin 5+ cells in the ICR (P = 0.03) and MCR (P = 0.06) was statistically significant. The mass of keratin 14+ cells in the ICR was significant (P = 0.002). Scale bar in A = 50 μm.
In the article entitled “Control of Th2-Mediated Inflammation by Regulatory T Cells” (Volume 177, pages 525–531 of the August 2010 issue), the first author's name was listed incorrectly. The author's name should have appeared as K. Venuprasad.
In the article entitled, “Proteasome Inhibitors Prevent Caspase-1-Mediated Disease in Rodents Challenged with Anthrax Lethal Toxin” (Volume 177, pages 735–743 of the August 2010 issue), the legend for Figure 3 contained errors. Specifically, the descriptions for panels Band C were switched. The corrected figure legend appears below:
Figure 3. Proteasome inhibitors block caspase-I-mediated LT killing of F344 macrophages. A: The proteasome inhibitors MG132, NPI-0052, and bortezomib were applied at the given concentrations to F344 BMMs treated with LT. Viability was established by WST-I assay 4 hours after LT-treatrnent. Data are represented as mean ± SD of N = 3, and representative data are shown from three independent experiments. B: NPI-0052 does not prevent caspase-I activation and cytolysis of F344 BMMs mediated by the Nalp3inducers LPS and nigericin. F344 BMMs were incubated with LT or LPS and nigericin in the presence of NPI-0052 and Boc-d-cmk for 4 hours. IL-Iβ processing was measured by Western blotting and cell survival was determined by LDH release. C: The proteasome inhibitor NPI-0052 does not block caspase-I directly. Lysates from LPS-primed 1344 BMMs were incubated with recombinant caspase-I in the presence of either NPI-0052 or Boc-d-cmk for 2 hours. Western blots were performed with an IL-Iβ antibody to monitor caspase-I activity. n.s. indicates nonspecific bands. Arrow points to mature IL-Iβ.
In the article entitled “Accelerated Lipofuscinosis and Ubiquitination in Granulin Knockout Mice Suggest a Role for Progranulin in Successful Aging” (Volume 177, pages 311–324), which appeared in the July 2010 issue, Dr. Charles A. Wuertzer was inadvertently omitted from the contributing authors. The list of contributing authors should have been listed as follows: Zeshan Ahmed, Hong Sheng, Ya-fei Xu, Wen-Lang Lin, Amy E. Innes, Jennifer Gass, Xin Yu, Charles A. Wuertzer, Harold Hou, Shuichi Chiba, Keitaro Yamanouchi, Malcolm Leissring, Leonard Petrucelli, Masugi Nishihara, Michael L. Hutton, Eileen McGowan, Dennis W. Dickson, and Jada Lewis.