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Suerth, V.

Publications and source records attributed to Suerth, V..

2 recordsLinked to original sources

Human placental stem cells induce a novel multiple myeloid cell-driven immunosuppressive program that ameliorates proinflammatory CNS pathology

Despite a growing interest in Amniotic Epithelial Cell (AEC)-based therapies, the immune responses triggered by AEC transplantation in vivo remain poorly characterized. In particular, how direct exposure to AECs within the central nervous system (CNS) shapes the local immune environment is currently unknown. Herein we describe a novel CNS- specific immunoregulatory pathway induced by intracisternal delivery of human AECs. Local immune responses induced by AECs in the brain led to recruitment of immunosuppressive Arginase 1+ (ARG1+) macrophages and a novel population of myeloid-derived suppressor cells with eosinophilic characteristics, which we term Eo- MDSCs. We further demonstrate that Eo-MDSCs produce Maresin 2 (MaR2), a specialized pro-resolving mediator (SPM) involved in the resolution of inflammation. In a mouse model of Multiple Sclerosis (MS), treatment of established disease with AECs induced immunological responses that resulted in reduced numbers of pathogenic macrophages and T helper (TH)17 cells, increased anti-inflammatory T cell subsets, and enhanced myelin phagocytosis, all of which led to functional recovery. These findings suggest that AEC therapy has the potential to target CNS-intrinsic inflammatory processes in MS, providing a strong rationale for translation into the clinic.

neuroscience↗

Disrupting microglial TGF-β signaling triggers region-specific pathology in the spinal cord

Transforming growth factor-{beta} (TGF-{beta}) signaling is critical for microglial maturation during development and the maintenance of microglial homeostasis in adulthood. It remains unclear whether regional susceptibilities to the loss of TGF-{beta} signaling in microglia also exist, and the contributing factors have yet to be identified. We find that deletion of Tgfbr2 on microglia leads to microglial activation and demyelination in mouse spinal cords, primarily in the dorsal column (DC). Tgfbr2-deficient microglia exhibit distinct transcriptomic changes, and those sorted from the DC display a more proinflammatory profile compared to those from the ventral column (VC) and grey matter (GM). Single nucleus RNA sequencing (snRNA-seq) of the spinal cord uncovers a microglial subtype that emerges exclusively following Tgfbr2 deletion (termed TGF{beta} signaling-suppressed microglia, TSM), exhibiting high expression of Mmp12, Gpnmb, Lgals3, Mgll, and Alcam, predominantly located in the DC. Phenotypically, disruption of microglial TGF-{beta} signaling results in behavioral deficits that are more severe in female and older mice, whereas young male mice are less affected. Mechanistically, we reveal a significantly higher level of TGF-{beta}1/TGFBR2 in the spinal cords of normal older mice compared to the young mice, with the DC region richer in genes of the TGF-{beta} signaling pathway than the VC and GM regions. This indicates that older mice and the DC region require more TGF{beta}1 to maintain tissue homeostasis and, reciprocally, are more responsive and sensitive to the disruption of TGF-{beta} signaling in microglia. Herein, we report a demyelinating disease with region-specificity and its susceptibility to the loss of microglial TGF-{beta} signaling with gender and age differences. Our findings contribute valuable information to our understanding of the importance of microglia in regulating myelin health, especially during the aging process.

neuroscience↗