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IL1A enhances TNF-induced retinal ganglion cell death
Katherine M Andersh1,2,3, Michael MacLean4, Gareth R Howell4
1Department of Ophthalmology, Flaum Eye Institute, University of Rochester Medical Center, Rochester, NY, United States.
Frontiers in Aging Neuroscience
|February 23, 2026
Summary
Interleukin-1 alpha (IL1A) sensitizes eyes to tumor necrosis factor (TNF)-induced retinal ganglion cell (RGC) death. This IL1A potentiation of TNF-induced RGC death is SARM1-dependent, highlighting a novel therapeutic target for glaucoma.
Area of Science:
- Ophthalmology
- Neuroscience
- Immunology
Background:
- Neuroinflammation plays a role in retinal ganglion cell (RGC) death in glaucoma.
- Interleukin-1 alpha (IL1A) and tumor necrosis factor (TNF) are implicated in this process, but IL1A's specific role is unclear.
Purpose of the Study:
- To investigate the role of IL1A in RGC survival and its interaction with TNF in glaucoma models.
- To determine the molecular mechanisms underlying IL1A and TNF-induced RGC death.
Main Methods:
- Intravitreal injections of IL1A, TNF, or both into wild-type, Jun-deficient, and Sarm1-deficient mice.
- Assessment of RGC survival via RBPMS immunostaining.
- Bulk RNA-sequencing to analyze molecular changes.
Main Results:
- IL1A alone did not cause RGC death, while TNF caused delayed RGC loss.
- Co-injection of IL1A and TNF led to rapid RGC death.
- IL1A+TNF-induced RGC death was SARM1-dependent but JUN-independent.
- Sarm1 deficiency protected RGCs from IL1A+TNF insult without altering neuroinflammation.
Conclusions:
- IL1A acts as a sensitizer to TNF-induced RGC death.
- The potentiation of TNF-induced RGC death by IL1A is mediated by SARM1.
- Targeting SARM1 may offer a therapeutic strategy for glaucoma.
