Igal Ifergan
University of Cincinnati, OH·Microbiology & Immunology
In multiple sclerosis (MS), immune cells enter the brain and spinal cord and attack myelin, the insulating coat around nerve fibers. Much attention has gone to T and B cells.
- Fields
Microbiology & Immunology
Neuroscience
- Topics
multiple sclerosis
experimental autoimmune encephalomyelitis
relapsing-remitting EAE
- Grants
- 2 known grants, through Jul 2027
What they work on
- 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.
- Overlay the mouse NK single-cell data onto public human MS datasets from blood, cerebrospinal fluid and lesions to test whether the same NK subsets exist in patients.
- Test whether mature NK cells promote and immature NK cells limit neuroinflammation, using co-culture of NK subsets with CNS slices and transfer of CFSE dye-labeled NK subsets into EAE mice.
- Test whether inflammatory signals at the neurovascular unit make brain endothelial cells and astrocytes produce Wnt proteins that steer myeloid antigen-presenting cells toward anti-inflammatory, repair-promoting responses.
- Determine how Wnt/β-catenin activation changes myeloid cell function, including PD-L1/PD-L2 levels and IL-1β, IL-6, IL-12 and IL-23 release, and whether Wnt manipulation can reduce CNS inflammation in vitro and in vivo.
More about the research
This work asks how other immune cells, and signals from the brain itself, push inflammation toward damage or toward repair. The two projects use experimental autoimmune encephalomyelitis (EAE), a mouse model of MS. One studies natural killer (NK) cells. The other studies how the Wnt signaling pathway calms the immune cells that present antigens to T cells.
Why it matters
People with multiple sclerosis need therapies that both stop brain inflammation and promote repair, including remyelination. Identifying which NK cell subsets are harmful or protective, and at which disease stage, could point to new treatment targets. Showing that brain-derived Wnt signals calm myeloid immune cells could suggest ways to boost this natural pathway to limit damage and support myelin repair.
Known grants
From NIH and NSF research grants. Labs often have other funding we can't see.
Closest labs
Booki Min
Northwestern University, IL·Microbiology & Immunology
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.
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.
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.
The school
University of Cincinnati: 18 labs on PI Pages, $740M a year on research, 275 research doctorates a year.
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