Pereira Lab
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cellreprolab.bsky.social
Pereira Lab
@cellreprolab.bsky.social
Cell Reprogramming in Hematopoiesis and Immunity, Lund University, Sweden. Tweets by Filipe Pereira (signed FP) and Malavika Nair (for Pereira lab). https://pereiralab.com/
We’re excited to share that our recent paper, “A combinatorial transcription factor screening platform for immune cell reprogramming”, has been selected for the cover of the January issue of Cell Systems!✨
January 21, 2026 at 5:16 PM
12) Take-home message: REPROcode is a versatile, single-cell-resolved platform to decode TF logic and engineer immune cells, from DC subsets to NK-like cells. REPROcode has broad future applications in cancer, autoimmunity, and tissue repair.
January 14, 2026 at 4:48 PM
11) Finally, we experimentally validated an NK reprogramming combination: TBX21, ETS1, NFIL3, and EOMES generated NK-like cells expressing CD56, NKG7, NCR1, GZMB, with functional capacity for degranulation and cytokine release.
January 14, 2026 at 4:47 PM
10) A decision tree trained on barcode counts and single-cell transcriptomes pinpointed key identity drivers: PU.1 at the root of reprogrammed cells, with KLF4 as a major early branch point, revealing a hierarchical TF map to guide immune cell reprogramming.
January 14, 2026 at 4:46 PM
9) Beyond cDC1: We uncovered TF modules for cDC2, pDC, macrophage, monocyte and NK trajectories. This highlighted the potential of REPROcode to generate immune heterogeneity.
January 14, 2026 at 4:45 PM
8) Programming immune diversity: Screening 48 TFs enriched in three DC subsets generated multiple immune phenotypes including myeloid and lymphoid, and extinguished fibroblast gene signatures. These patterns were reproduced across three experiments.
January 14, 2026 at 4:45 PM
7) Beyond cell fate, we could also use REPROcode to identify factors that modify cDC1 cell states when co-expressed with PIB:
• IκB-α/β (NFKBIA/B) → immature cDC1
• MXD1, ID2 → immunostimulatory/mature cDC1
• BCL6, IRF7 → CCR7⁺ migratory cDC1
January 14, 2026 at 4:44 PM
6) The levels of identified co-factors also matter: GATA2 increased fidelity in a narrow window, as higher levels reduced reprogramming efficiency and XCR1 expression. GFI1B boosted efficiency at higher levels. This reveals distinct mechanisms of cooperation of GATA2 and GFI1B with PIB.
January 14, 2026 at 4:44 PM
5) We showed that stoichiometry matters: high PU.1 + high BATF3 + intermediate IRF8 = best cDC1 induction from human fibroblasts or multiple cancer cells.
January 14, 2026 at 4:43 PM
4) Barcode recovery was robust and evenly distributed in reprogrammed cells. On the optimization side, we observed that more TFs, lower MOI, and higher cell recovery sharpened inference from large pools. Our meta-analysis shows this boosts accuracy for identifying instructive TFs.
January 14, 2026 at 4:43 PM
3) By applying multiplexed TF libraries (9, 22, and 42 factors), we reconstructed PIB-mediated (PU.1, IRF8, BATF3) cDC1 reprogramming, enabling resolution of minimal TF combinations and stoichiometries and revealing GATA2 and GFI1B as key enhancers of lineage fidelity.
January 14, 2026 at 4:42 PM
2) What's REPROcode? A barcoded, arrayed lentiviral library of 408 immune TFs (now available through Addgene - www.addgene.org/Filipe_Perei...) + scRNA-seq that links which reprogramming TFs a cell receives to the identity it acquires. With no extra barcode PCR steps!
January 14, 2026 at 4:42 PM
1) Cell reprogramming holds great promise for next-generation immunotherapies, but combinatorial logic of TF network remains a challenge. We developed REPROcode to systematically interrogate TF combinations at single-cell resolution while resolving cell identity and state.
January 14, 2026 at 4:41 PM
In a game of Mancala, each move strategically redistributes pieces mirroring how TF combinations direct immune cell fate. We present REPROcode to uncover these combinatorial rules providing a roadmap to reprogram cells into defined immune identities. Illustration: Lilith Lawrence
January 14, 2026 at 4:40 PM
1/4 Great to share that our lab was awarded a research grant from the Mats Paulsson Foundation for Research, Innovation and Societal Development for the project “Advancing Reactive Tumor-Infiltrating Lymphocyte Therapy with Cellular Reprogramming”.
October 24, 2025 at 2:47 PM
1/2 Sharing exciting news! ✨
Our recently published paper “Anchored screening identifies transcription factor blueprints underlying dendritic cell diversity and subset-specific anti-tumor immunity” has been selected for the cover of the October issue of Immunity!
@cp-immunity.bsky.social
October 14, 2025 at 3:41 PM
2/2 Yet, dendritic cells had another go with Abigail Altman, who won the Best Poster Award with "Transcription factor blueprints underlying dendritic cell diversity", now out in Immunity (www.cell.com/immunity/ful.... Congrats to both! It's great to have our contributions recognized!
September 17, 2025 at 1:08 PM
1/2 Celebrating a double win!✨ Yesterday, at the Lund Stem Cell Center (LSCC) retreat, Ervin Ascic was awarded the Article of the Year Award with our Science paper "In vivo dendritic cell reprogramming for cancer immunotherapy" (www.science.org/doi/10.1126/...)
September 17, 2025 at 1:06 PM
We are proud to announce that Ervin Ascic successfully defended his PhD yesterday – with the special honor of Nobel Laureate James Allison as opponent! ✨
Ervin’s work makes a strong contribution, showing that in vivo dendritic cell reprogramming is paving the way toward the clinic.
September 5, 2025 at 8:29 AM
13/17 🧩 Our results propose that ETS–IRF pairwise interactions constitute the foundation upon which any DC identity may be built and help define the drivers of DC divergence, advancing our understanding of DC specification and heterogeneity.
August 29, 2025 at 4:20 PM
12/17 ⚖️ Surviving mice remained tumor-free upon rechallenge, showing durable immune memory. This finding points toward patient-tailored DC subsets as a new immunotherapy avenue.
August 29, 2025 at 4:20 PM
11/17 🐭 Importantly, in melanoma (YUMM1.7) and breast cancer (EO771), in vivo reprogramming towards different iDC subsets drove orthogonal anti-tumor responses, mirroring the natural DC responsiveness on these tumors.
August 29, 2025 at 4:19 PM
10/17 💉 In B16 melanoma tumor models, adoptive transfer of iDCs slowed growth and improved survival through distinct mechanisms: iDC2s boosted CD8+ and CD4+ T cells; iLDCs promoted myeloid infiltration.
August 29, 2025 at 4:18 PM
9/17 ⚙️ Mechanistically, each TF triad had different chromatin engagement modes and co-bound subset-specific genes early on, showing that DC subset divergence is set in motion at the very start of reprogramming.
August 29, 2025 at 4:17 PM
8/17 ⚔️ Functionally, iDC2s resembled inflammatory cDC2Bs with features of interferon-stimulated cDC2s, activating CD8+ T cells via antigen uptake, processing, and cross-presentation, demonstrating real immune potential.
August 29, 2025 at 4:17 PM