đŹDynamics of immune responses to pathogens and tumors. đSan Raffaele Scientific Institute & University, Milan @SanRaffaeleMI @MyUniSR
Joined March 2011
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30 Jun 2025
1/ đ¨ Hot off the press in @NatImmunol: CD4âş T cells can license Kupffer cells to rescue dysfunctional CD8âş T cells in the liver. Hepatitis B virus (HBV) infection is just the proving groundâthis is a paradigm shift in tissue immunity. nature.com/articles/s41590-0⌠đ§ľ(1/11)
2/ Chronic HBV infection was the perfect stress test: intrahepatic CD8âşâŻT cells are primed yet quickly stall. How to reignite them has been a major interest of our lab. (2/11)
3/ Preâactivated helper CD4âşâŻT cells solve the puzzle. They skip lymph nodes and head straight to the liver, where they form intimate triads with Kupffer cells (KCs), the resident macrophages patrolling sinusoids. (3/11)
4/ Through CD40LâCD40 contact, those helpers reâprogram KCsâturning tolerant scavengers into potent APCâlike cytokine factories. Itâs onâsite immune engineering, not remote coaching. (4/11)
5/ Licensed KCs release a twoâpart cocktail:
⢠ILâ12 expands the helper pool
⢠ILâ27 wakes up dysfunctional CD8âşâŻT cells, restoring effector molecules and metabolic vigor. (5/11)
6/ Dendritic cells? Dispensable. Secondary lymphoid organs? Surgically removed or pharmacologically blockedâhelp still flows. Immunity can be fabricated in situright inside the parenchyma. (6/11)
7/ Remove KCs and the circuit collapses; block CD40L or ILâ27 and CD8âşâŻT cells relapse into lethargy. The essential loop is:
CD4âŻT cell â KC â ILâ27 âCD8âŻT cell. (7/11)
8/ ILâ27 isnât just necessaryâitâs sufficient. Recombinant ILâ27 revived antiviral CD8âşâŻactivity in mice and superâcharged HBVâspecific T cells from patients. (8/11)
9/ Why care beyond HBV? Tapping a CD4âILâ27 axis could be a universal key to reâarming liverâresident CD8âşâŻT cells against infections and cancer (9/11)
10/ The work reframes âCD4 helpâ: not a lymphânode pep talk but an onâsite renovation that overrides local tolerance. Therapeutics that mimic KC licensing could deliver potency where itâs needed and spare the rest of the body. (10/11)
11/ Kudos to Valentina Venzin, Cristian Beccaria, all members of the @IannaconeLab & collaborators for charting this intrahepatic circuit. Expect Kupfferâcell licensing and ILâ27 to enter conversations on cancer immunotherapy, vaccines and beyond. Thoughts welcome! đ
@ImmunoPodcast @profvrr @ERC_Research @EMBO @EMBO_YIP @ArmeniseHarvard
@AIRC_it @MyUniSR @SanRaffaeleMI
(11/11)
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Pleased to have contributed to this new @ScienceMagazine paper on how lymphoid tissue chemokines limit CD8âş T cell priming duration to preserve T cell functionality. Congrats to @LukasAltenburg2 and Jens Stein! science.org/doi/10.1126/scieâŚ
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Iannacone Lab retweeted
Apr 9
Review @NatRevImmunol @Kubes_Lab @FGinhoux @iannaconelab
Kupffer cells in liver homeostasis and disease: from immune sentinels to metabolic gatekeepers
nature.com/articles/s41577-0âŚ
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Great fun to write this review on Kupffer cells with @FGinhoux and @Kubes_Lab, covering origin, diversity and roles in immunity and metabolism, now out @NatRevImmunol. Huge credit to Bruna Araujo David, @frarro1 and Camille BlĂŠriot for driving this work. rdcu.be/fckoZ
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Iannacone Lab retweeted
Abortive infection: T cells as early, antibody-independent defenders dlvr.it/TRrTjj
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Neutralizing antibodies are not the whole story. In @NatRevImmunol, we highlight an alternative mode of protection: T cells can eliminate infection at its earliest stage, before it becomes detectable. We term this âabortive infectionâ
rdcu.be/fbq8p
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Implications:
⢠T cells can act at inception, not just during clearance
⢠Standard readouts (serology/PCR) miss these events
⢠True exposure and immunity are likely underestimated
â We need to measure what T cells actually do
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This calls for a shift in vaccine design:
⢠target early, conserved viral proteins
⢠build tissue-resident immunity
⢠combine antibodies and T cells
Great collaboration with Leo Swadling, @ValeFuma91 and @maini_lab
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Excited to organize @KeystoneSymp Tissue and Spatial Immunology with @LeilaAkkari1 and Hai Qi in February 2027! Join us to explore emerging research in Banff! keysym.us/KSSpatialImmune27 #KSSpatialImmune27 pic.x.com/UmTB6SW1x7
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Join us for the 2026 GRC Immunochemistry and Immunonbiology "Immune Circuitry and Molecular Pathways in Tissue Homeostasis, Infection, and Disease" in beautiful Barcelona. June 28 - July 3, 2026. Great lineup of speakers! grc.org/immunochemistry-and-âŚ
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Jan 24
Great story from the @NieswandtLab in @ScienceMagazine: uncovering a non-classical platelet mechanism that drives inflammation via integrin- and tetraspanin-rich tethers. A fresh angle on thrombo-inflammation. Happy to be part of this work!
science.org/doi/10.1126/scieâŚ
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Jan 23
Very clever approach in this must-read paper from @IdoAmitLab! đĽ
Jan 22
What if we could turn the tumorâs deadliest tricks against it?
New @Cancer_Cell: Tumor-antigen-independent targeting of solid tumors by armored macrophage-directed anti-TREM2 CAR T cells. Led by @GalYagel, @D_Rimini & @MVLocquenghien (1/15)
cell.com/cancer-cell/abstracâŚ
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20 Dec 2025
1/ New from our lab đ§Ş
ARTC2 blockade is widely used to protect tissue Tregs â but when is it truly essential, and for which subsets?
2/ In this @EurJImmunol update, we dissect the subset-specific and context-dependent effects of ARTC2 blockade on hepatic Treg recovery.
3/ At steady state, ARTC2 blockade has a selective benefit: it markedly improves recovery and preserves phenotype of CD44^mid (less-activated) Tregs, while having minimal impact on effector-like eTregs.
4/ During liver inflammation, ARTC2 blockade becomes critical: it boosts overall Treg yield and prevents phenotypic distortion â again with the strongest effect on CD44^mid Tregs.
5/ Key insight: hepatic Treg subsets are not equally sensitive to ARTC2âP2RX7 activation.
Less-activated, tissue-resident Tregs are preferentially lost or skewed without protection.
6/ Practical takeaway đĄ
⢠Studying activated/eTregs at steady state? ARTC2 blockade may be optional.
⢠Profiling CD44^mid Tregs or working in inflammatory settings? ARTC2 blockade is essential.
7/ Bottom line: this work reframes ARTC2 blockade from a default reagent to a rational, cost-effective experimental choice.
8/Â Proud of the team â led by @CaitlinAAbbott, with @VioletteMouro and colleagues â for turning a technical challenge into actionable guidance for the field.
9/ Read the paper here đ onlinelibrary.wiley.com/doi/âŚ
And stay tuned â exciting new discoveries on liver Tregs are coming soon đđ§Ź
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21 Dec 2025
Thanks to Chiara Perucchini and Chiara Vespari for their critical contribution
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25 Nov 2025
Thrilled to contribute to this landmark consensus effort led by @Masopust_Vezys and @rafiahmed_lab. A major step toward clearer, shared T cell nomenclature for the field.
18 Nov 2025
Guidelines for T cell nomenclature bit.ly/48258LX
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23 Nov 2025
Honoured to see our @NatImmunol study highlighted in a thoughtful @JHepatology commentary on the IL-27/Kupffer cell axis in chronic HBV. A great summary of why local tissue immunity matters â and wonderful to see the field engaging with our work.
Paper: nature.com/articles/s41590-0âŚ
Commentary: journal-of-hepatology.eu/artâŚ
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Iannacone Lab retweeted
20 Nov 2025
New review out! đ 20 years after its discovery, with @iannaconelab we decided to bring together what we currently know about this cytokine and how it shapes CD8 T cell responses. A small contribution to make sense of a field that is moving fast đ
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20 Nov 2025
New review out in @TrendsImmuno! With @ValentinaVenzin, we revisit IL-27 as a central regulator of CD8âş T cell fate â integrating insights from infection, cancer, and autoimmunity, and outlining its therapeutic potential. sciencedirect.com/science/arâŚ
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Iannacone Lab retweeted
19 Nov 2025
Excited to share our study @CellCellPress introducing a novel class of macrophage-targeted immunocytokines (MiTEs) that engage myeloid, T and NK cells to boost anti-tumor immunity in solid tumors. Led by @MVLocquenghien, @PascaleZwicky & @CuriousKX (1/16)
cell.com/cell/abstract/S0092âŚ
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