I of course want to thank all of the collaborators that made this possible: our departmental and clinician colleagues at @mayoclinic.org (there are so many that I won't be unfair here and name some of them) as well as Ronaldo Francisco Jr. from @harvard.edu for helping us in the big data analyses.
Finally, I was particularly proud of co-leading this with Igor. This was, frankly, originally his idea. I was a bit concerned that this was going to be a distraction for him (it is not his primary project), but it turned out to be a great idea! This is a great sign of his scientific maturity.
This was also a great example of what I believe science should be: it started with somewhat unconventional observations, which led us to try to understand these observations. In other words, WE adapted to the data we saw.
This work also highlighted a possible unconventional way by which P2RX7 regulates Treg biology. We are still not entirely sure how unique this is for lung tumors but we certainly did not find this in ectopic tumor models!
This work is important for many reasons. It shows a possible important mechanism by which Tregs maintain and exert suppression of immune responses in lung cancer, opening the possibility for using P2RX7 inhibitors in the clinic. This is something we will want to test in the future.
Mechanistically, we found that P2RX7 drove the transcriptional and protein expression of CTLA-4 in Tregs. We are currently studying how this receptor can regulate other pathways in Tregs (future studies!). Finally, Igor found that P2RX7 blockade can revert the Treg suppression in these tumors!
This was somewhat puzzling to us, because one of the canonical effect of P2RX7 is to induce the apoptosis of Tregs. However, through the use of lung tumor models, Igor found that P2RX7 is necessary for Tregs to exert their suppressive capacity in lung tumors!
...Igor explored publicly available clinical data and found that high P2RX7 expression is tied to poor lung cancer prognosis in patients. We then explored publicly available spatial transcriptomics data and found that this is possibly due to the presence of P2RX7-expressing regulatory T cells!
In this work, we wanted to investigate how this purinergic receptor can impact the immune responses to lung cancer. We often look at how P2RX7 can positively impact protective T cell responses, mostly focusing on effector T cells. However...
Now that the final version is online, I am happy to share our latest paper! Igor Santiago-Carvalho, our talented postdoc, led this paper together with myself. Please check it out! Below, a mini tutorial:
aacrjournals.org/cancerimmuno...
Nature story about the appropriations "minibus" bill and NIH
www.nature.com/articles/d41...
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I'll be heading (together with other LIDS members) to IMMUNOLOGY2026™ from April 15–19, 2026! I'm looking forward to connecting with old and new friends from the immunology community. If you're thinking about going, register today! i.snoball.it/p/31TbLKBz/b/1
#IMMUNOLOGY2026 #AAI2026
T cell nomenclature diagram titled "T cell nomenclature: from subsets to modules" shows existing and alternative modular T cell nomenclature with examples. Text includes descriptions of T cell types and functions.
A Consensus Statement in Nature Reviews Immunology clarifies the existing subset-based nomenclature for T cells. It also proposes an alternative modular nomenclature that is designed to be brief and flexible and to avoid ambiguity and unwanted implications. go.nature.com/3Xzfoqb #immunosky 🧪
I’d like to thank all the co authors, especially Caio Salgado who spearheaded this project, as well as my collaborator Dr. Fonseca. We hope this counterintuitive IL33 mediated effect can help explain at least some of the aspects of the so called “hygiene hypothesis”
In this work, we discovered that gut exposure to enterotoxigenic E. coli (the ones that cause travelers diarrhea 😬) or its heat labile toxin can protect mice from lung type 2 allergy, which is linked to lung ILC2s losing their function. Paradoxically, this effect occurs BECAUSE of gut IL33 release!
Hi everyone! This is the official account of the LIDS (formerly known as Borges da Silva lab - I didn’t want to have a lab named after me). I wanted to start this account by sharing our latest preprint, a collaboration with Denise Fonseca (USP-Brazil)! This is our first IL33 (and allergy) story
Escherichia coli-induced gut IL-33 release inhibits lung type 2 allergic responses https://www.biorxiv.org/content/10.1101/2025.11.07.687219v1
