JCI Issues Corrigendum for TREM-2 Tuberculosis Study After Supplemental Figure Error
The TREM-2 tuberculosis paper in JCI has been corrected after the authors identified an error in one of its supplemental images. In Supplemental Figure 14G, the H&E image for the TREM-2+ group was incorrect, and the online supplemental PDF has now been updated with the correct figure.
This is a narrow correction, but it sits inside a broader immunology paper that drew attention for placing TREM-2 in an unexpected position during Mycobacterium tuberculosis infection: not only as a modulator of innate immune signaling, but as a contributor to CD4+ T cell activation and Th1 immunity. A mislabeled or incorrect histology image does not rewrite the study’s central mechanistic claims, yet it does matter for the integrity of the visual record that supports them.
The corrected article was published as a corrigendum in 2026, with the underlying research article originally appearing in 2021. The journal lists the original citation and the corrigendum separately, and the version history now reflects the updated supplemental material.
Why the Supplemental Image Mattered in a Th1 Immunity Paper
The parent study proposed that TREM-2 expression on CD4+ T cells is induced by M. tuberculosis infection in humans and mice, and that this expression tracks with T cell activation and an effector memory phenotype. In that framework, tissue images are not decorative. They help anchor the experimental story in morphology, inflammation, and cellular context, especially when the paper is arguing for a host-defense pathway that shapes the immune response to infection.
The study also described a signaling route that diverged from the canonical myeloid-cell model. In CD4+ T cells, TREM-2 interacted with the CD3ζ-ZAP70 complex and with the IFN-γ receptor, leading to STAT1/4 activation and T-bet transcription. The authors further used infection models involving reconstituted Rag2–/– mice and CD4+ T cell–specific TREM-2 conditional knockout mice to support the conclusion that TREM-2 promoted a Th1-mediated host defense against tuberculosis.
A single incorrect H&E panel does not alter those experimental claims by itself. But it can affect how readers assess the tissue-level appearance of the TREM-2+ group, and that is why journals correct even isolated supplemental errors rather than leaving them buried in an appendix.
One incorrect image is enough to demand a corrected record.
The Scientific Record and the Limits of a Corrigendum
Corrigenda occupy a specific place in medical publishing. They are not retractions, and they are not formal challenges to the core conclusions of a paper. Instead, they repair the literature when an error is identified after publication. In this case, the correction is limited to the Supplemental Figure 14G H&E image for the TREM-2+ group, and the authors state that the supplemental PDF has been updated online with the correct figure.
For investigators reading the original tuberculosis paper, the correction means the supplemental evidence now matches the intended dataset presentation. For clinicians and translational scientists, the practical consequence is simpler: the mechanistic narrative should be interpreted using the corrected supplemental material rather than the earlier version.
That matters most in fields like infection and inflammation, where visual pathology, flow cytometry, signaling biology, and conditional knockout models often converge to support a causal argument. A supplemental histology panel may appear secondary at first glance, yet in an immunology paper it can help readers judge whether the cellular phenotype aligns with the rest of the experimental readout.
TREM-2 Remains Positioned as an Immune Signaling Node in Tuberculosis
The corrected notice does not revise the original mechanistic framing of TREM-2. The study still places the receptor in a proinflammatory context during tuberculosis infection, where it is associated with CD4+ T cell activation, effector memory differentiation, and Th1-biased host defense. The pathway described in the paper is unusual because it links TREM-2 to T cell signaling machinery rather than limiting it to its more familiar myeloid-cell biology.
That cross-lineage signaling concept is what made the paper notable in the first place. In macrophages and other innate cells, TREM-2 has long been discussed as a regulator of inflammatory tone. In this study, its role extends into adaptive immunity, where interaction with the CD3ζ-ZAP70 complex and the IFN-γ receptor is presented as a route toward STAT1/4 activation and T-bet transcription. Those steps sit squarely in Th1 biology, the arm of immunity most relevant to intracellular pathogens such as Mycobacterium tuberculosis.
The correction leaves that biology intact while tightening the documentary record. In a field that depends on reproducible imaging and carefully matched supplementary data, that is not a minor administrative detail. It is part of how confidence is maintained in the chain from image to mechanism to host-defense model.
What Readers Should Take From the Correction
The updated notice gives readers a clear instruction: use the corrected supplemental PDF. The original article remains part of the literature, but the specific image in Supplemental Figure 14G should now be read in its corrected form. No new cohort, no new endpoint, and no new mechanistic claim was introduced in the corrigendum itself.
For a tuberculosis immunology paper, that restraint is appropriate. The journal corrected a defined visual error, the authors acknowledged it, and the updated supplemental file now accompanies the study. The record is more accurate because the correction is explicit rather than implicit, and future readers will not have to guess whether the image they are viewing is the final version.
The remaining question for the field is not whether TREM-2 participates in the immune response to tuberculosis; the original paper already argued that it does. The more immediate issue is how this receptor integrates with T cell activation pathways across infection and inflammation, and whether those signaling interactions can be leveraged without destabilizing host defense elsewhere. The corrected image does not answer that question, but it restores the visual evidence supporting the paper that raised it.