Booki Min
Northwestern University, IL·Microbiology & Immunology
Immune responses need brakes as well as accelerators. One of those brakes is Lag3 (lymphocyte activation gene 3), a surface protein that quiets the cell carrying it.
- Fields
Microbiology & Immunology
Neuroscience
- Topics
Lag3
lymphocyte activation gene 3
inhibitory co-receptor
- Grants
- 2 known grants, through Oct 2028
What they work on
- Determine how Lag3, an inhibitory surface co-receptor, lets Foxp3+ regulatory T cells suppress autoimmune neuroinflammation, using mice with the Lag3 outer domain, cytoplasmic tail or KIEELE motif deleted only in Tregs.
- Identify the molecular pathways through which Lag3 signaling shapes the metabolism and suppressive capacity of regulatory T cells, building on evidence that the cytokine IL-27 induces Lag3 in these cells.
- Test whether deleting Lag3 in microglia, the brain's resident immune cells, changes microglial maintenance in healthy mice and alters the course of experimental autoimmune encephalomyelitis.
- Work out the mechanism by which Lag3 drives microglia toward anti-inflammatory subsets during autoimmune inflammation of the central nervous system.
More about the research
Drugs that block Lag3 are being developed to unleash T cells against tumors, but Lag3 also sits on cells whose job is to calm inflammation. Two projects here ask what Lag3 does in those calming cells during autoimmune attack on the brain and spinal cord. One looks at regulatory T cells, the immune system's peacekeepers; the other at microglia, the brain's own resident immune cells. Both rely on mouse models of experimental autoimmune encephalomyelitis (EAE), an autoimmune inflammation of the central nervous system.
Why it matters
Because Lag3-blocking antibodies are already in clinical use as checkpoint drugs, knowing how Lag3 supports peacekeeping Tregs and brain microglia matters for predicting side effects and for designing new approaches. The work could point to therapeutic strategies aimed at Lag3 or the signals it triggers for controlling chronic autoimmune inflammation of the brain and spinal cord.
Known grants
From NIH and NSF research grants. Labs often have other funding we can't see.
Closest labs
Igal Ifergan
University of Cincinnati, OH·Microbiology & Immunology
Characterize mature (CD27- CD11b+) and immature (CD27+ CD11b-) natural killer cell subsets in the brain and spinal cord across stages of relapsing-remitting EAE, a mouse model of MS, using single-cell RNA sequencing.
Mingnan Chen
University of Utah, UT·Pharmacology
Determine why a depleting anti-PD-1 antibody delays diabetes in early insulitis but accelerates it in late insulitis in NOD mice, profiling pancreatic islets and systemic immune cells by single-cell RNA sequencing and flow cytometry before and after treatment.
David Rothstein
University of Pittsburgh, PA·Microbiology & Immunology
Define the gene activity of TIM-4+ effector B cells and the signaling pathways, including IL-23 and IL-17, that switch on their inflammatory program while suppressing IL-10 and regulatory function, using RNA sequencing and quantitative PCR.
The school
Northwestern University: 71 labs on PI Pages, $1.3B a year on research, 536 research doctorates a year.
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