Search bioRxiv⌕ Search

bioRxiv · 10.1101/2025.04.23.650273

GM-CSF production by immune cells in steady state and autoimmune neuroinflammation mapped using fate reporting mice

Abstract

The full GM-CSF expression spectrum in immune cells remains unclear, while CD4{square} T cells are the primary source. Using novel GM-CSF reporter/fate reporter transgenic mice, we tracked ongoing and past (YFP+) GM-CSF expression in various immune cells. GM-CSF was produced by diverse immune cells, including CD4+, CD8+, {gamma}{delta} T, NK, B, and CD11b+ cells, with expression patterns varying by cell type and organ with liver CD4+ T cells and NK cells showing the highest expression history in both naive and mice with EAE. GM-CSF expression was transient and permanently lost in most cells over time. In a mouse model of multiple sclerosis, effector memory CD4{square} T cells were the dominant CNS GM-CSF source, with higher expression than in other organs. CD4+YFP+ T cells, strongly expressing CXCR6, produced multiple cytokines. Transcriptomic analysis showed distinct gene expression profiles in effector memory CD4+ T cells compared to naive cells. YFP{square} Tregs represent functionally distinct subsets mirroring effector Th cells, expressing cytokines associated with Th lineages, especially during neuroinflammation. These findings identified distinct GM-CSF cellular sources across organs, highlighting a transient tissue microenvironment influence on GM-CSF production linked to CXCR6 expression.

Source connections

Explore related subjects

Keep this discovery

Explore connections, maps & timelines

BibTeXRIS

Azizi, G., Rasouli, J., Naziri, H., Gonzalez, M. V., Garifallou, J., Zhang, G.-X., Ciric, B., Rostami, A.. 2025-04-26. GM-CSF production by immune cells in steady state and autoimmune neuroinflammation mapped using fate reporting mice. https://doi.org/10.1101/2025.04.23.650273

Cite the original work for its findings. Save a collection to share your selection of sources.

KEEP EXPLORING

Related preprints

Common viral infections seed regionally distinct resident memory T cells in the human CNS

T cells persist in the central nervous system (CNS) and can drive both protection and neurological disease. How these cells are organized in humans and what they recognize is largely unknown. Here, we profiled CD8 T cells across anatomically distinct CNS regions, obtained through on-site autopsies and temporal lobe resection surgeries, using single-cell RNA sequencing, paired T cell receptor sequencing, and DNA-barcoded tetramers. Resident memory T cells (TRM) specific for Epstein-Barr virus, cytomegalovirus, influenza A, and SARS-CoV-2 were identified across CNS compartments. Anatomical location was the strongest correlate of TRM cell state, with leptomeningeal cells adopting a cytokine-poised TRM program, whereas brain TRM cells were transcriptionally restrained. Cells of the same clonotype spanned tissues yet adopted local transcriptional states. Viral specificity added another layer of TRM heterogeneity with GZMK/GZMA-expressing EBV-specific populations and interferon-stimulated gene signatures in SARS-CoV-2 and Influenza A-specific cells. The human CNS thus harbors regionally distinct CD8+ TRM shaped by common viral exposures.

immunology↗

A regulatory T cell signature provides a shared molecular basis for the therapeutic window of opportunity in rheumatic disease

Rheumatic diseases, including rheumatoid arthritis (RA), spondyloarthritis (SpA) and osteoarthritis (OA), show distinct phenotypes yet respond to overlapping therapies, implicating shared immune mechanisms. In the Transimmunom cohort, we profiled peripheral blood from 240 individuals (47 healthy, 44 OA, 91 RA, 58 SpA) across deep immunophenotyping, immunoproteomics and Treg-Teff transcriptomics. Single-layer analyses revealed broader Treg than Teff remodeling, along with a shared pattern of reduced activated Tregs and expanded Helios+ Tregs across all diseases, alongside a decrease in functional Treg subpopulations, including CTLA4+ and CD45RA- Tregs. In RA specifically, LAG3+ Tregs were also expanded. Combining omics layers outperformed single-layer approaches for disease classification. Among individual layers, Treg transcriptomes were most discriminative, and integration uncovered disease-specific programs. Unsupervised clustering identified a cross-disease cluster independent of activity, treatment and age, mapping to early disease (<= years) and dominated by a Treg dysfunction-associated program. These results provide a biological rationale for the therapeutic "window of opportunity" concept and duration-stratified Treg-directed trials.

immunology↗

Inhibitory Fc Receptor sets a time limit on macrophage response to IgG

Antibodies engage both activating Fc Receptors and the inhibitory receptor Fc{gamma}RIIB. Why macrophages need a dedicated inhibitory receptor rather than simply tuning activating receptor signaling is unclear. Using DNA-based chimeric receptors and in silico modeling, we independently controlled activating and inhibitory Fc Receptors. We found that Fc{gamma}RIIB imposed a time limit on macrophage phagocytosis and ERK signaling. The time limit is due to activating Fc Receptors converting PI(4,5)P2 to PI(3,4,5)P3, which is subsequently converted to PI(3,4)P2 by Fc{gamma}RIIB. This leads to a pulse of active signaling, which is sufficient for phagocytosis of small bacteria-sized targets but not phagocytosis of large targets and TNF secretion. Unlike engaging Fc{gamma}RIIB, reducing activating Fc Receptor signaling decreased initiation of phagocytosis, the speed of PI(3,4,5)P3 generation, and the amplitude of ERK signaling. Our results demonstrate that Fc{gamma}RIIB controls the duration of IgG signaling, while the activating Fc Receptors control sensitivity.

immunology↗