The Colonna Lab

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

[Julia Belk @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/

https://t.co/5jtMEvvNMd

[The Colonna Lab @TheColonnaLab]

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.

https://t.co/IEzw44YYdB

[Julia Belk @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/
https://t.co/BuHdVk1V2I

[Immunity @ImmunityCP]

Online now: Age- and tissue-dependent diversity of human plasmacytoid dendritic cells uncovers a cycling subset dominant in early life and cancer https://t.co/keKZA21DjG

[The Colonna Lab @TheColonnaLab]

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. https://t.co/O0UJ5O02sa

[The Colonna Lab @TheColonnaLab]

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!

https://t.co/rObe8n6N00

[The Colonna Lab @TheColonnaLab]

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!

https://t.co/toBkTydEpT

[Science Magazine @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.

📄: https://t.co/jMTIzVznEV
#SciencePerspective: https://t.co/h1aL5tdltT

[Science Immunology @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: https://t.co/4VpXUvc3ll

[The Colonna Lab @TheColonnaLab]

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).

https://t.co/1KwQTbPdlm

[Immunity @ImmunityCP]

Online now: Immunity in Alzheimer’s disease: From mechanisms to therapies https://t.co/Y9IKiNDKb7

[The Colonna Lab @TheColonnaLab]

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: https://t.co/hPe4uypDtO

[Science Immunology @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. https://t.co/gPykZ9U3Yw

[The Colonna Lab @TheColonnaLab]

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.

https://t.co/CKN3hhV9rz

[The Colonna Lab @TheColonnaLab]

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!
https://t.co/f3HaHEODzz

[The Colonna Lab @TheColonnaLab]

Check out Research Briefing for our recent paper in Nature Immunology @DuSiling
https://t.co/UjsyIt79Vi

[Siling Du @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.
https://t.co/39kxODSumy

[The Colonna Lab @TheColonnaLab]

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.

https://t.co/k2PsmXO9mX

[The Colonna Lab @TheColonnaLab]

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. https://t.co/a2iQeoo1n4

[The Colonna Lab @TheColonnaLab]

Find the referenced papers below:
Brown: https://t.co/emADApLMLM
Mucida: https://t.co/CIcqHoP0Xx
Littman: https://t.co/F4yBTXweBJ
Gardner: https://t.co/R5amWicVLb
Schraml: https://t.co/HgE9kK3lHL
Colonna: https://t.co/2RLR96OSYf

[The Colonna Lab @TheColonnaLab]

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.https://t.co/emADApLMLM

[The Colonna Lab @TheColonnaLab]

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!