University of Glasgow professor Foo Yew “Eddy” Liew, a Fellow of the Royal Society, has retracted a paper in Cellular Immunology because it duplicated one of his earlier papers in the Proceedings of the National Academy of Sciences (PNAS).
Here’s the notice for “Expression and function of Toll-like receptor on T cells:”
This article has been retracted at the request of the authors. This article is a duplication of a paper that has already appeared in Proc Natl Acad Sci U S A. 2004 Mar 2;101(9):3029–34. Epub 2004 Feb 23. The authors would like to apologize to the readers for this error on their part.
The now-retracted paper has been cited 60 times, according to Thomson Scientific’s Web of Knowledge, while the PNAS version, “TLR2 is expressed on activated T cells as a costimulatory receptor,” has been cited 210 times.
The Cellular Immunology abstract:
Toll is the founder of a group of pattern recognition receptors, which play a critical role in the innate immunity in Drosophila. At least 13 distinct Toll-like receptors (TLRs), recognising pathogen-associated molecular pattern (PAMPs), have now been identified in humans. Most investigations on TLRs have focused on cells of the innate system. We report here that naïve human T cells expressed high levels of cell surface TLR2 after activation by anti-T cell receptor (TCR) antibody and interferon-alpha. Activated cells produced elevated levels of cytokines in response to the TLR2 ligand, bacterial lipopeptide (BLP). Furthermore, CD4(+)CD45RO(+) memory T cells from peripheral blood constitutively expressed TLR2 and produced IFNgamma in response to BLP. BLP also markedly enhanced the proliferation and IFNgamma production by CD45RO(+) T cells in the presence of IL-2 or IL-15. Thus, TLR2 serves as a co-stimulatory receptor for antigen-specific T cell development and participates in the maintenance of T cell memory. This suggests that pathogens, via their PAMPs, may contribute directly to the perpetuation and activation of long term T cell memory in both antigen dependent and independent manner.
The PNAS abstract:
Toll is the founder of a group of pattern recognition receptors that play a critical role in the innate immunity in Drosophila. At least 10 distinct Toll-like receptors (TLRs), recognizing pathogen-associated molecular patterns, have now been identified in humans. Most investigations on TLRs have focused on cells of the innate system. We report here that naïve human T cells expressed high levels of cell-surface TLR2 after activation by anti-T cell receptor antibody and IFN-alpha. Activated cells produced elevated levels of cytokines in response to the TLR2 ligand, bacterial lipopeptide. Furthermore, CD4(+)CD45RO(+) memory T cells from peripheral blood constitutively expressed TLR2 and produced IFN-gamma in response to bacterial lipopeptide, which also markedly enhanced the proliferation and IFN-gamma production by CD45RO(+) T cells in the presence of IL-2 or IL-15. Thus, TLR2 serves as a costimulatory receptor for antigen-specific T cell development and participates in the maintenance of T cell memory. This suggests that pathogens, via their pathogen-associated molecular patterns, may contribute directly to the perpetuation and activation of long-term T cell memory in both antigen-dependent and independent manner.
Liew tells us it was the pseudonymous Clare Francis who alerted his team to the error:
We then consulted the Editors of Cellular Immunology and together we decided to withdrawn this article. I have to point out that there was no misleading information involved.
Liew has had two other recent retractions, one of a 1995 paper whose lead author was found by the U.S. Office of Research Integrity to have falsified data, and another involving Alirio Melendez. The Melendez paper also has Damo Xu, a co-author on the Cellular Immunology paper, as a co-author.
Update, 11:30 a.m. Eastern, 7/22/13: Added “no” to quote from Liew, who erred in his email to us earlier but corrected it after we’d posted:
Sorry, what I meant was there was NO misleading information involved. That is, there was no misleading data involved.
Reblogged this on The Firewall.
What purpose do these annoying “reblogged on” notices serve, other than promotional?
No idea. If you know how to disable then I’m all ears.
Done. They shouldn’t show up anymore.
“Liew tells us it was the pseudonymous Clare Francis who alerted his team to the error.” Amazing! The PNAS paper has five co-authors, the CI paper has three. All three co-authors of the CI paper also co-authored the PNAS paper. Still, an “error” was committed. By whom? How? What about the senior author, the group boss? Did he not read both manuscripts before his name was put on them?
Indeed. I would consider the different author list as “mileading information” if the papers are duplicates.
And why not these ones here, with a 67.43% ratio of similarity in the abstract:
ST2 is an inhibitor of interleukin 1 receptor and Toll-like receptor 4 signaling and maintains endotoxin tolerance PUBMED ID 15004556
AND
A novel negative regulator for IL-1 receptor and Toll-like receptor 4
PUBMED ID 15585304
A very similar case.
Reference: http://dejavu.vbi.vt.edu/dejavu/duplicate/75/
Maybe worth registering these on Pubpeer?
I sent to them, let’s see.
PUBMED ID 15585304 is a short Immunology Letters paper that does not contain any data and seems to be a mini-review. If it concerns the findings in PUBMED ID 15004556 perhaps it is not surprising that many of the words in the abstract coincide. Not my field (and full of mysterious acronyms) so I was discouraged from digging further into the text.
The Immunology Letters paper is listed as a “review”, and the Nature Immunology paper is a primary article. The review (which appeared later) does not cite the earlier Nature Immunology paper. The first author of the Nature Immunology paper (Dr Elizabeth K Brint) is not one of the authors of the Immunology Letters review, but she is thanked in the acknowledgments. Not only the abstracts, but also the concluding paragraphs are nearly identical.
Could you pelase try to send it to any trustable source that will check it “officially”?
In reply to DEUS ex MACHINA July 24, 2013 at 4:28 am
That’s the job of the journal editors.
http://publicationethics.org/files/u2/01B_Redundant_Published.pdf
http://pubpeer.com/publications/95A6AC62211AD6CDB7C37C7949B3EB
The role of innate mediators in inflammatory response Molecular Immunology 38 (2001) 887–890
Role of interleukin 15 and interleukin 18 in inflammatory response Ann Rheum Dis 2002;61(Suppl II):ii100–ii102
Role of interleukin 18 in rheumatoid arthritis Ann Rheum Dis 2003;62(Suppl II):ii48–ii50
The role of innate cytokines in inflammatory response Immunology Letters 85 (2003) 131
What did you see there Webb, could you please clarify and expose on pubpeer, please?
Whatever, the point is:
ST2 is an inhibitor of interleukin 1 receptor and Toll-like receptor 4 signaling and maintains endotoxin tolerance PUBMED ID 15004556
AND
A novel negative regulator for IL-1 receptor and Toll-like receptor 4
PUBMED ID 15585304
I read both, the Immunology letters is ridiculously a copy of the Nat Immunol data. Nothing new or expanding the info presented in the original paper.
If someone is eager to put it in the editor’s table, go for it. The contact must be done somehow!
Why a negative vote? Things like that must be discussed or am I wrong?