University clears leading dermatology lab head of misconduct as authors issue two corrections
Felicitas Riedel, a legal officer for the university, tells Retraction Watch that the
…Committee for Scientific Misconduct of the Philipps-University Marburg closed the matter and submitted its results to the President of the University who in the meantime after examination consented with it.
Prof. Dr. Michael Hertl is officially and completely exculpated. Based on an accurate fact-finding lasting for months the Committee adjudicated that Mr. Hertl neither committed any Scientific Misconduct himself nor overlooked such in his department by negligence. The latter means: if committed by a member of his group, Mr. Hertl could not foresee, recognize or prevent it. Please note that my permit to disclose personal data does not cover anyone but Mr. Hertl. Information on any other person involved cannot be given. Mr. Hertl was also completely exonerated within the framework of a disciplinary complaint from any accusation of breach of official duty.
The findings, of course, leave open the possibility that someone in Hertl’s lab may have committed misconduct.
Both new corrections appear in the Journal of Immunology. Here’s one:
Veldman, C., A. Höhne, D. Dieckmann, G. Schuler, and M. Hertl. 2004. Type I regulatory T cells specific for desmoglein 3 are more frequently detected in healthy individuals than in patients with pemphigus vulgaris. J. Immunol. 172: 6468–6475.
Fig. 2 of this article shows identical FACS images for the mIgG1 isotype control for CD25, CCR4, and TGF-β (all mouse IgG1-PE) as well as HLA-DR, CD45RO (both mouse IgG2a-PE), and CCR7 (rat IgG2a-PE), which is due to the use of inappropriate isotype controls by the first author of the study. Because we cannot rule out that observed differences in the expression patterns of HLA-DR, CD45RO, and CCR7 may be less significant when compared to the appropriate Ab isotype controls, these data have now been omitted in the revised Fig. 2, below. In addition, we have inserted an FACS image for CTLA-4 expression of the Th2 cells from the same original experiment. CTLA-4 expression was detected by a Cytochrome-labeled Ab (clone BNI3.1). The major observation of Fig. 2 that desmoglein 3-reactive Tr1 cells, but not Th2 cells, express glucocorticoid-induced TNFR and TGF-β is not affected by this revision. In Figs. 3, 4, and 5, proliferative T cell responses are expressed as mean cpm [3H]TdR ± SD. The authors apologize to the scientific community for any inconvenience these errors may have caused.
And here’s the other:
Veldman, C., A. Pahl, S. Beissert, W. Hansen, J. Buer, D. Dieckmann, G. Schuler, and M. Hertl. 2006. Inhibition of the transcription factor Foxp3 converts desmoglein 3-specific type 1 regulatory T cells into Th2-like cells. J. Immunol. 176: 3215–3222.
In Fig. 3, our group recently discovered that the FACS data for SCR2 at 0.4 μM were incorrectly labeled as 0.2 μM, and that the data for SCR2 at 0.4 μM were generated in an unrelated experiment and incorrectly inserted by the first author of the study. In addition, the first author used inadequate isotype controls for glucocorticoid-induced TNFR family-related receptor (GITR) (polyclonal IgG) that were identical to the isotype controls for CD4 (mIgG1). Even though we have shown in an independent experiment that desmoglein (Dsg)3-reactive Tr1 cells express GITR and that treatment with Foxp3 AS2 but not Foxp3 SCR2 leads to downregulation of GITR expression by Tr1 cells, we prefer to omit Fig. 3 based on the described inaccuracies. The overall message of the study, namely the observation that Tr1 cells treated with Foxp3 AS2 lose their suppressor function, gain a proliferative phenotype, and start to secrete the T cell growth factor, IL-2, is not affected by the errors of Fig. 3. Moreover, we have not directly linked expression of GITR or CTLA-4 to the suppressor function of the Tr1 cells. Neither have we found convincing evidence that the secretion of IL-10 and TGF-β by the Tr1 cells exclusively mediates their suppressor function since IL-10 and TGF-β secretion was also not altered by Foxp3 AS2 treatment. Because the ability of the Tr1 cells to produce IL-2 was directly linked to the loss of suppressor function, we speculate that the Dsg3-reactive Tr1 cells suppress T cell responses by the consumption of exogenous IL-2. The major finding of the study (i.e., that antisense-mediated loss of Foxp3 is directly associated with the loss of suppressor function) has been confirmed by a recent, independent study (Hansmann et al. 2012. J. Immunol. 188: 1275–1282) showing that downregulation of Foxp3 in Treg cells leads to Th2 differentiation. In Figs. 4 and 6, proliferative T cell responses are expressed as mean cpm [3H]TdR ± SD. The authors apologize to the scientific community for any inconvenience these errors may have caused.
The corrections match concerns raised by the Abnormal Science blog, as we noted last year, although the post in which the blog noted the issues seems to no longer be available. The papers have been cited 65 and 32 times, respectively, according to Thomson Scientific’s Web of Knowledge.