immunologist, mother and wife of a partner in life and science. love T cells and bugs, always questioning and doubting
Milano, Lombardia
Joined January 2012
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federica facciotti retweeted
🧬 È online la campagna #BiUniCrowd “Microbi chef: possiamo mettere il tumore a dieta?”
L’obiettivo è studiare il legame tra microbiota e #tumore al colon per capire il ruolo dei nutrienti nella crescita tumorale
Dona ora👉 ideaginger.it/progetti/micro…
federica facciotti retweeted
🔬 Fondazione AMICI Italia rinnova il proprio impegno a favore della ricerca scientifica sulle Malattie Infiammatorie Croniche Intestinali, con il nuovo Consiglio di Amministrazione:
ℹ️ 𝐋𝐞𝐠𝐠𝐢 𝐥’𝐚𝐫𝐭𝐢𝐜𝐨𝐥𝐨 𝐜𝐨𝐦𝐩𝐥𝐞𝐭𝐨👉 amici.tv/48z3Zg5
federica facciotti retweeted
Federica Facciotti, from University of Milano Bicocca, focuses on how the gut microbiota interacts with immune activation, shaping both chronic inflammatory intestinal disorders and oncology, particularly colorectal cancer.
microbiomepost.com/microbiot…
federica facciotti retweeted
We are hiring!! 📢 A one-year Master's thesis is available in the lab starting from October 2025. All at the intersection of mechanistics of self-renewal, stem cells and cancer. Links to apply below
federica facciotti retweeted
Will it ever be possible to find a definitive cure for #inflammatoryboweldiseases? Find out most recent developments towards this ambitious goal in our latest review edited by @dnoviello_93 Chiara Amoroso @federicafacciot and Maurizio Vecchi. sciencedirect.com/science/ar….
federica facciotti retweeted
Our work on the sexual dimorphism of colorectal cancer is finally out in Oncoimmunology!
A huge thanks to @GeorgiaLattanzi @Federic16207690, @epiangie and the whole @LoungeTcell lab. Grateful for the support from @AIRC_it and #AMMI Donne per la salute
rb.gy/j5tre2
Pure joy is when your collaborators receive recognition for their work 🎉
Chiara Amoroso @fcaprioli76 and the @LoungeTcell team best award for our #fmt study in #IBD at the 238 Congress of the Falk Foundation @policlinicoMI
Oops we did it again! #iNKT cells are functionally shut down by bugs (here Porphiromonas gingivalis) in #colorectal #cancer. Soon a summary of the study, now Thanks to @epiangie @GeorgiaLattanzi @stratifnc , the whole @LoungeTcell and @AIRC_it
doi.org/10.1080/19490976.202…
#BtBsPUB in Gut Microbes journal "Porphyromonas gingivalis fuels colorectal cancer through CHI3L1-mediated iNKT cell-driven immune evasion" by #StratiLab_BtBs #FacciottiLab_BtBs #BaeriLab_BtBs & co-authors. #BtBsUNIMIB @unimib tandfonline.com/doi/full/10.…
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Lab moving ongoing
✔️-4 done
✔️-80 done
✔️-20 in progress
✔️10 years of reagents, lab books, various stuff (some of not certain utility)
✔️car packed
✔️some tears
✔️new beginnings ahead at @BtBsUNIMIB
✔️@LoungeTcell alive&kicking!
In the rush of the return home from #UEGWeek we did not celebrate the achievement of @dnoviello_93, Who won the Best National Abstract award. @fcaprioli76 clinical and myself research super-proud mentors! Grande Daniele🌟
Fun and inspiration, plus cool science and rigorous clinical science #UEGWeek2024
We proudly presented the work of @federicaperillo and jointly coordinated with @stratifnc on CAC patients and the consequences of deregulated T cells activation
Finally, this paper is dedicated to the memory of our dear colleague Nicolas Barnich who recently passed away. His untimely departure is a profound loss to the scientific community and to all who had the privilege of knowing him.
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A big thanks goes to all the people involved in the study, from @gabrijejuni , to X-less Moira Paroni, to @fcaprioli76 @dnoviello_93 @policlinicoMI @LaStatale @unimib for their huge effort on this exciting project. We also thank @FondCariplo that financially supported us
Summary: our findings indicated that the transdifferentiation of pTh17 cell is strongly driven in CD patients by AIEC determinants, such as rfaP or ybaT , generated within AIEC-infected DCs, and presented to cTh17 cells together with very high IL-23 levels.
Clinical Significance: 1) YbaT is ubiquitously found across all E. coli pathotypes, differently from other virulence factors like FimH. 2) Targeting of ybaT and rfaP inhibits pTh17 generation without affecting protective Th17 cells.
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rfaP is a LPS core heptose(I) kinase modifying the LPS inner core.Its absence alters structure and stability of the outer membrane (👉different antigens!). ybaT is an aminoacid permease involved in the glutamate dependent copper (Cu) tolerance (👉less stress resistance!)
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To exclude putative polar effects of transposon insertion in our mutants, we generated individual isogenic deletion mutants in rfaP and ybaT genes, confirming our data with DC (persistence and IL23 secretion) and Th17 (transdifferentiation)
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Functional validation with DCs and Th17 cells. Six mutants impairedd IL23 secretin, but ΔybaT (T59.F12) and to a lesser extent ΔrfaP (T12.G9 and T45.G12) mutants drastically impaired also the skewing of cTh17 into pTh17 cells.
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The DNA sequencing after rescue cloning revealed that the transposon insertions in these 13 selected LF82 mutants occurred within genes involved in a few specific pathways including metabolic processes, stress response, LPS and capsule biosynthesis.
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