The Colonna Lab

RT @juliabelk: 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/

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.

RT @juliabelk: 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/

RT @ImmunityCP: Online now: Age- and tissue-dependent diversity of human plasmacytoid dendritic cells uncovers a cycling subset dominant in early life and cancer

What defines human pDC diversity? Our newest work led by @UlezkoAlina in @ImmunityCP uncovers a complex landscape shaped by age and tissue niche, including a cycling pDC subset that declines with age but persists in the BM & expands in malignant BPDCN.

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!

Our study is out in @ScienceMagazine! It shows that CAR-expressing astrocytes (CAR-A) can recognize and clear amyloid aggregates, reducing pathology and restoring microglial homeostasis in AD models. Led by Yun Chen, Alex Liu and @khainotkaiorky!

RT @ScienceMagazine: 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. 📄: #SciencePerspective:

RT @SciImmunology: 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:

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).

RT @ImmunityCP: Online now: Immunity in Alzheimer’s disease: From mechanisms to therapies

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:

RT @SciImmunology: 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.

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.

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!

Check out Research Briefing for our recent paper in Nature Immunology @DuSiling

RT @DuSiling: 🧵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.

Our new study by @DuSiling reveals how CSF1R mutations in adult-onset leukoencephalopathy with axonal spheroids and pigmented glia (ALSP) disrupt glial homeostasis. Key roles for oligodendrocytes, astrocytes & STAT3 signaling.

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.

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.

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!

Find the referenced papers below: Brown: Mucida: Littman: Gardner: Schraml: Colonna: