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Article | Open Access

sIL-2RA Exacerbates Multiple Sclerosis by Activating Microglia and Upregulating Fc Receptors on Microglia

Jingfei Shi#, Yi Ding#, Hui Lu( )
Department of Neurology and China-America Institute of Neuroscience, Xuanwu Hospital, Capital Medical University, Beijing, China

#These authors contributed equally to this work

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Abstract

Objective

Multiple sclerosis (MS) is a chronic inflammatory demyelinating disease of the central nervous system (CNS). Soluble interleukin-2 receptor alpha (sIL-2Rα) has been implicated in MS pathogenesis, but its mechanisms remain unclear. This study investigates how sIL-2Rα exacerbates MS by modulating microglial activation and antibody-dependent cellular cytotoxicity (ADCC) in an experimental autoimmune encephalomyelitis (EAE) mouse model.

Methods

Female C57BL/6J mice were induced with EAE and treated with sIL-2Rα. Clinical symptoms, histopathology, and molecular changes were analyzed. Microglial activation was assessed via immunohistochemistry, Western blot, and RNA sequencing. In vitro, ADCC-mediated oligodendrocyte injury was evaluated using Fc receptor inhibition and PI3K-Akt pathway blockade.

Results

sIL-2Rα accelerated EAE onset and severity, increasing microglial M1 polarization and CNS inflammation. RNA-seq revealed PI3K-Akt pathway activation, upregulating Fc receptors (FcγR) on microglia, which enhanced ADCC against oligodendrocytes (p < 0.001). Inhibiting FcγR or PI3K-Akt reduced oligodendrocyte damage.

Conclusion

sIL-2Rα exacerbates MS by activating microglia via the PI3K-Aktaxis, promoting ADCC and demyelination. Targeting this pathway may offer novel therapeutic strategies for MS.

Keywords

Multiple sclerosissoluble interleukin-2 receptor αmicroglial activationphosphatidylinositol 3-kinase–protein kinase B signaling (PI3K-Akt) signaling pathwayantibody-dependent cellular cytotoxicity

References

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BIOCELL
Volume 50 Issue 3,
March 2026
Article number: 7
DOI: 10.32604/biocell.2026.073956

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Shi J, Ding Y, Lu H. sIL-2RA Exacerbates Multiple Sclerosis by Activating Microglia and Upregulating Fc Receptors on Microglia. BIOCELL, 2026, 50(3): 7. https://doi.org/10.32604/biocell.2026.073956

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Received: 29 September 2025
Accepted: 12 January 2026
Published: 23 March 2026
© The Author 2026.

This work is licensed under a Creative Commons Attribution 4.0 International License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.