We study innate immunity with a focus on ILCs, macrophages, and DCs. The account is led by trainees. @wusm_pathology @WUSTLmed

St. Louis, MO
The Colonna Lab retweeted
The transcription factor MAF is known from human genetics to be important in Alzheimer’s disease, but its precise function within the brain has been unclear. Our latest, out today in @CellCellPress, dissects the role of MAF in brain macrophages. 1/ cell.com/cell/fulltext/S0092…
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New paper from the Colonna lab! cMAF is a key regulator of BAM identity and drives communication with brain arteries via IGF1. We show that this cMAF-dependent program in BAMs supports cerebrovascular function in mice and is protective against AD. cell.com/cell/fulltext/S0092…
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The Colonna Lab retweeted
Gaining therapeutic access to the human brain is one of the biggest unsolved problems in biomedical science. Today @nature, we uncover a massive influx of immune cells into the human brain during aging, revealing that the brain is more accessible than previously thought. 1/ nature.com/articles/s41586-0…
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Excited to share our latest work in J Exp Med! We identify LINGO4 as a key regulator of ILC3 fitness, IL-22 production and microbiota homeostasis, with major impact on host defense against enteric infection. Check it out! doi.org/10.1084/jem.20252632
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The Colonna Lab retweeted
Genetically altered astrocytes that express chimeric antigen receptors offer a promising immunotherapy system capable of clearing accumulations of amyloid-β in the brains of mice—a hallmark pathological feature of #AlzheimersDisease, according to a new study in Science. 📄: scim.ag/3NjPIfP #SciencePerspective: scim.ag/4rgI1oL
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The Colonna Lab retweeted
Platelet-derived growth factor D (#PDGFD) binds to PDGFRβ in #ILC3s in mice and NKp44 in human ILC3s, promoting divergent innate immune responses following intestinal infections. @TheColonnaLab Learn more in Science #Immunology: scim.ag/4aXJmL1
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Excited to share our new work in @SciImmunology, led by @zefachi! Mesenchymal cells produce PDGF-D during colitis, driving species-specific ILC3 programs: via PDGFRβ in mice (IL-22, repair) and NKp44 in humans (type I response, pathogen clearance). science.org/eprint/EFDJ3BJRF…
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How do microglia and T cells shape Alzheimer’s? We review the stage-specific roles of innate and adaptive immunity, from genetic risk factors to precision therapies. Is the immune system a guardian or a saboteur? check out in our review in Immunity: authors.elsevier.com/a/1mgnQ…
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The Colonna Lab retweeted
A new Science #Immunology study pinpoints the developmental origin of a distinct group of #DendriticCells that express the transcription factor #RORγt and highlights molecular players that regulate this process. scim.ag/45vKMue
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Excited to share that our work by @PatFernRod & @TongWu99 is published: RORγt⁺ DCs are a distinct lymphoid-derived lineage whose development is controlled by REV-ERBα/β, PRDM16 and PU.1, enabling pTreg induction and protection from Th2-skewed responses. rb.gy/lyvce8
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Our new study led by Bishan Bhattarai shows that circadian proteins REV-ERBα/β protect gut health by maintaining ILC3 homeostasis. Without them, ILC3s turn into IFNγ+ ILC1s, fueling inflammation. Chick it out! nature.com/articles/s41590-0…
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The Colonna Lab retweeted
🧵1/ Excited to share my first publication from the @ColonnaLab in @NatImmunol! We investigated how mutations in the human CSF1R gene disrupt microglia and impair white matter integrity in a rare but devastating neurodegeneration called ALSP. nature.com/articles/s41590-0…
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Congrats to @KedmiRanit’s group! RORγt⁺ APCs prime food-specific pTregs and induce oral tolerance. Infection or food poisoning temporarily bypasses this, allowing CD8αβ T cell responses to mimicked food antigens without breaking long-term oral tolerance. nature.com/articles/s41586-0…
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Big shoutout to Brown’s group: IRF8-dependent TC are essential for inducing food-specific pTregs & establishing oral tolerance! In line with recent work from Mucida’s, Littman’s, Gardner’s, and our group highlighting the role of RORγt⁺ APC in this process.rb.gy/rej77q
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As RORγt⁺ APC gain attention for their tolerogenic roles, Schraml’s group also highlights their inflammatory potential. Key questions remain: How are RORγt⁺ APC specified? Are eTAC and RORγt⁺ DC distinct or the same? What dictates tolerance vs. inflammation? Fast-moving field!
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