Monocyte-plasma cell communication characterizes treatment-associated peripheral immune remodeling in Guillain-Barré syndrome.

Background: Guillain -Barré syndrome (GBS) is an acute immune-mediated polyradiculoneuropathy involving multifaceted pathogenic mechanisms. Although humoral immunity is central to GBS pathogenesis, longitudinal changes in peripheral immune circuits across symptomatic disease and clinical recovery remain incompletely understood at single-cell resolution. Methods: We performed longitudinal single-cell RNA sequencing of peripheral blood mononuclear cells collected during the symptomatic GBS and clinical recovery phases from a patient with GBS. Changes in immune cell composition, transcriptional programs, intercellular communication, and gene regulatory networks were examined, with particular attention to plasma cells, monocytes, B cells, and putative double-negative T cells (DNTs). Results: Plasma cells, monocytes, and putative DNTs exhibited stage-dependent transcriptional remodeling. During the GBS phase, plasma cells exhibited increased secretory and IgG-associated programs, consistent with enhanced antibody-producing activity. Monocytes represented higher relative proportion and showed enrichment of antigen-presentation and inflammatory pathways. Cell -cell communication analysis indicated stronger inferred BAFF and APRIL signaling from monocytes toward B cells and plasma cells during the GBS phase, suggesting a potential monocyte contribution to humoral activation. Regulatory network analysis identified SPI1-associated activity within the inflammatory monocyte program. In parallel, putative DNTs showed comparatively higher inferred outgoing cytokine signaling together with enrichment of ribosome biogenesis and protein synthesis pathways. During recovery, plasma cell secretory signatures were attenuated. B cells upregulated memory- and regulatory-associated genes, inflammatory monocyte programs diminished, and inferred DNT-associated cytokine signaling was lower in the recovery sample, accompanied by receptor-mediated and adhesion-related transcriptional programs. Conclusion: Collectively, these findings provide a longitudinal single-cell view of peripheral immune remodeling in GBS and highlight a stage-associated monocyte -B-cell regulatory axis and differences in DNT-associated inferred cytokine signaling between the GBS and recovery samples.