Dual-targeting CSF1R signaling attenuates neurotoxic myeloid activation and preserves photoreceptors in retinitis pigmentosa

Abstract Retinitis pigmentosa (RP), a group of inherited retinal diseases characterized by progressive photoreceptor degeneration, features prominent microglial activation and monocyte-derived macrophage infiltration. While colony-stimulating factor 1 receptor (CSF1R) shows diverse roles in regulati...

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Main Authors: Jiangmei Wu, Jing Zhang, Bin Lin
Format: Article
Language:English
Published: BMC 2025-07-01
Series:Journal of Neuroinflammation
Subjects:
Online Access:https://doi.org/10.1186/s12974-025-03525-0
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author Jiangmei Wu
Jing Zhang
Bin Lin
author_facet Jiangmei Wu
Jing Zhang
Bin Lin
author_sort Jiangmei Wu
collection DOAJ
description Abstract Retinitis pigmentosa (RP), a group of inherited retinal diseases characterized by progressive photoreceptor degeneration, features prominent microglial activation and monocyte-derived macrophage infiltration. While colony-stimulating factor 1 receptor (CSF1R) shows diverse roles in regulating microglial survival and behaviors in various neurodegenerative diseases, its functional significance in RP pathogenesis remains unclear. In this study, we observed upregulated CSF1R signaling specifically within disease-associated myeloid cells in the rd10 mouse model of RP. Targeted intervention via intravitreal CSF1R neutralizing antibodies and systemic PLX5622 administration achieved reduced myeloid proliferation and pro-inflammatory cytokine production and greater photoreceptor survival. Notably, CSF1R potentiation using recombinant IL-34 or CSF1 exacerbated neuroinflammation and accelerated photoreceptor degeneration. Mechanistic investigations revealed that infiltrating monocyte depletion by clodronate liposomes significantly reduced macrophage infiltration and preserved visual function. Using CX3CR1CreER/+/R26iDTR/+/rd10 mouse model, we observed that diphtheria toxin-mediated microglia ablation preserved retinal function. Overall, our findings demonstrate the prominent role of CSF1R in neurotoxic myeloid activation in the context of RP. Our results provide preclinical proof-of-concept that dual targeting of retinal and peripheral CSF1R pathways may offer a mutation-agnostic therapeutic strategy for inherited retinal degenerations.
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spelling doaj-art-e3eac9dc16b14e21976309a28c2f79b62025-08-20T03:05:11ZengBMCJournal of Neuroinflammation1742-20942025-07-0122111710.1186/s12974-025-03525-0Dual-targeting CSF1R signaling attenuates neurotoxic myeloid activation and preserves photoreceptors in retinitis pigmentosaJiangmei Wu0Jing Zhang1Bin Lin2School of Optometry, The Hong Kong Polytechnic UniversitySchool of Optometry, The Hong Kong Polytechnic UniversitySchool of Optometry, The Hong Kong Polytechnic UniversityAbstract Retinitis pigmentosa (RP), a group of inherited retinal diseases characterized by progressive photoreceptor degeneration, features prominent microglial activation and monocyte-derived macrophage infiltration. While colony-stimulating factor 1 receptor (CSF1R) shows diverse roles in regulating microglial survival and behaviors in various neurodegenerative diseases, its functional significance in RP pathogenesis remains unclear. In this study, we observed upregulated CSF1R signaling specifically within disease-associated myeloid cells in the rd10 mouse model of RP. Targeted intervention via intravitreal CSF1R neutralizing antibodies and systemic PLX5622 administration achieved reduced myeloid proliferation and pro-inflammatory cytokine production and greater photoreceptor survival. Notably, CSF1R potentiation using recombinant IL-34 or CSF1 exacerbated neuroinflammation and accelerated photoreceptor degeneration. Mechanistic investigations revealed that infiltrating monocyte depletion by clodronate liposomes significantly reduced macrophage infiltration and preserved visual function. Using CX3CR1CreER/+/R26iDTR/+/rd10 mouse model, we observed that diphtheria toxin-mediated microglia ablation preserved retinal function. Overall, our findings demonstrate the prominent role of CSF1R in neurotoxic myeloid activation in the context of RP. Our results provide preclinical proof-of-concept that dual targeting of retinal and peripheral CSF1R pathways may offer a mutation-agnostic therapeutic strategy for inherited retinal degenerations.https://doi.org/10.1186/s12974-025-03525-0CSF1RProliferationNeuroinflammationPhotoreceptor degenerationMicrogliaMacrophages
spellingShingle Jiangmei Wu
Jing Zhang
Bin Lin
Dual-targeting CSF1R signaling attenuates neurotoxic myeloid activation and preserves photoreceptors in retinitis pigmentosa
Journal of Neuroinflammation
CSF1R
Proliferation
Neuroinflammation
Photoreceptor degeneration
Microglia
Macrophages
title Dual-targeting CSF1R signaling attenuates neurotoxic myeloid activation and preserves photoreceptors in retinitis pigmentosa
title_full Dual-targeting CSF1R signaling attenuates neurotoxic myeloid activation and preserves photoreceptors in retinitis pigmentosa
title_fullStr Dual-targeting CSF1R signaling attenuates neurotoxic myeloid activation and preserves photoreceptors in retinitis pigmentosa
title_full_unstemmed Dual-targeting CSF1R signaling attenuates neurotoxic myeloid activation and preserves photoreceptors in retinitis pigmentosa
title_short Dual-targeting CSF1R signaling attenuates neurotoxic myeloid activation and preserves photoreceptors in retinitis pigmentosa
title_sort dual targeting csf1r signaling attenuates neurotoxic myeloid activation and preserves photoreceptors in retinitis pigmentosa
topic CSF1R
Proliferation
Neuroinflammation
Photoreceptor degeneration
Microglia
Macrophages
url https://doi.org/10.1186/s12974-025-03525-0
work_keys_str_mv AT jiangmeiwu dualtargetingcsf1rsignalingattenuatesneurotoxicmyeloidactivationandpreservesphotoreceptorsinretinitispigmentosa
AT jingzhang dualtargetingcsf1rsignalingattenuatesneurotoxicmyeloidactivationandpreservesphotoreceptorsinretinitispigmentosa
AT binlin dualtargetingcsf1rsignalingattenuatesneurotoxicmyeloidactivationandpreservesphotoreceptorsinretinitispigmentosa