Microbiota-derived peptide and autoimmune heart inflammation: a tale of missing data
Papers published in the journal Science are required to go through a thorough, high-level vetting procedure. But making mistakes is human. Because they are both human, reviewers and editors make mistakes frequently, much to the chagrin of scientists and the delight of postdocs participating in journal clubs. In addition, & nbsp,
Here is an illustration of a paper that managed to get past the Science vetting procedure. It asserts that MYH6, a protein found in the heart muscle, cross-reacts with peptides from particular commensal microbiota species, resulting in autoimmune heart inflammation. Its excellent Figure 1 demonstrates how MYH6-specific TCR transgenic mice on a germ-free background with no microbiota are shielded from heart autoimmunity.
Additionally, they demonstrated that the reintroduction of microbiota into germ-free mice increases their susceptibility to heart inflammation, much like that of microscopic + mice.
The authors then made an effort to pinpoint the species of microbiota that cause this inflammatory condition. Cross-reactive galactosidase (- gal ) mimic peptides in Bacteroides thetaioteomicron ( B. tha) and B. fascis were found to have a high similarity to MYH6 during an in silico search.
The authors even introduced Bacteroides thetaioteomicron ( B. tha) lacking the – gal into germ-free TCR transgenic mice. It appears that the authors have checked every box required for high-quality research up to this point. However, as shown in figure 1, they do not display survival data comparing Bacteroides thetaioteomicron ( B. tha ) with and without the – gal gene. They merely demonstrated how the accumulation of MYH6 – T cells in the heart tissue is altered by the absence of the Bacteroides thetaioteomicron.
Why then don’t the authors display the survival data of germ-free MYH6 TCR transgenic mice that have been colonized with the Bacteroides thetaiomicron -/+ – gal gene? Isn’t it their hypothesis’ most significant finding? Where were editors and reviewers searching?
