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Engineering an inhibitor resistant human CSF1R variant for microglia replacement [InVivo_RNA]

ABSTRACT: iPSC-derived hematopoietic progenitor cells expressing either the wildtype or G795A CSF1R variant were xenotransplanted into neonatal mice and subsequently aged for two months to compare in vivo gene expression differences between the two CSF1R genotypes.

ORGANISM(S): Homo sapiens

PROVIDER: GSE220214 | GEO | 2022/12/21

REPOSITORIES: GEO

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			Action	DRS
		Other
	GSE220214_Chadarevian_2022_G795A_InVivo_RawSeqCounts.tsv.gz	Tabular
	GSE220214_Chadarevian_2022_G795A_InVivo_VSTSeqCounts.tsv.gz	Tabular

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Engineering an inhibitor resistant human CSF1R variant for microglia replacement [InVitro_RNA]

Project description:iPSC-derived microglia expressing the wildtype, G795A, or G795C CSF1R variants were generated in vitro and treated with either DMSO or Plexxicon 5622 in order to compare the gene expression differences exising between genotypes at baseline or following CSF1R inhibtion.

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Engineering an inhibitor resistant human CSF1R variant for microglia replacement

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Project description:Recent advances in cell-based therapies have demonstrated therapeutic safety and efficacy for a variety of diseases. However, significant challenges remain in their development for the treatment of neurological disorders. Preclinical studies have explored microglial replacement strategies utilizing bone marrow transplantation and CSF1R-inhibitor (CSF1Ri) treatment. However, these approaches often require highly invasive strategies and result in engrafted cells that remain transcriptionally and functionally distinct from microglia. To assess less invasive microglia replacement strategies capable of preserving microglial ontogeny, we developed a Csf1r-G793A knockin mouse. We found G793A mice develop typical microglial densities and peripheral hematopoietic populations which exhibit broad CSF1Ri resistance enabling widespread microglia replacement following direct intraparenchymal injection or bone marrow transplantation. Furthermore, we demonstrate that widespread microglia replacement can be achieved via less invasive intracisternal delivery of CSF1Ri-resistant murine and iPSC-derived human microglia. Together with the accompanying study by Lombroso and colleagues, our findings demonstrate that G793A mice provide a robust and broadly applicable source of engraftable donor microglia and peripheral macrophages for the preclinical investigation of microglia replacement strategies.

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Project description:Chimeric antigen receptor (CAR) T cells have revolutionized the landscape of cancer therapy, demonstrating unprecedented success in treating relapsed or refractory blood cancers. Previous studies of the mechanisms underlying the interactions and responses of CAR T cells and their targets have focused on the activation of CAR T cells and attempted to optimize CAR design to increase efficacy, while ignoring tumors and their responses to CAR ligation. We evaluated the signaling of a second-generation, ligand-based CAR built from the colony-stimulating factor 1 (CSF1) ligand to target the CSF1 receptor (CSF1R) on CSF1R-expressing target cells, and compared it to a conventional single-chain variable fragment (scFv)–based CAR against the B-cell antigen CD19 using stable isotope labeling by amino acids in cell culture (SILAC) co-culture with phosphotyrosine (pY) enrichment and liquid chromatography–tandem mass spectrometry (LC–MS/MS).. We showed that ligation of CSF1R-expressing THP-1 cells with CSF1R-CAR T cells stimulated CSF1R-like signaling in the THP-1 cells, whereas no target cell signaling response was observed after the ligation of CD19-CAR T cells with target Raji cells. In experiments with small-molecule inhibitors of the tyrosine kinase Lck, actin polymerization, and CSF1R, we found that CAR-induced CSF1R signaling in THP-1 cells depended exclusively on the kinase activity of CSF1R with no participation from T cell activation. Consistently, CSF1R-CAR T cells promoted THP-1 cell growth at low effector-to-target (E:T) ratios but prevented THP-1 cell growth at high E:T ratios. Our data provide evidence for an unintended consequence of CARs: CAR-induced signaling in cancer cells. These data may have broad implications for the choice of CAR antigen for optimal clinical efficacy.

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