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CNS-Native Myeloid Cells Drive Immune Suppression in the Brain Metastatic Niche through Cxcl10 [R07_CCR2Cx3cr1B]

ABSTRACT: We performed CITE-seq (10x Genomics-based) to profile and compare the transcriptomes and cell surface expression of immune epitopes in the brains and blood of different transgenic mice (Cx3cr1+/-; Cx3cr1-/-; CCR2+/-; CCR2-/-) during homeostasis or brain metastasis. We sequenced a total of eight different samples. We created an antibody pool consisting of 35 different antibodies and stained each sample individually with this antibody pool. Then, we stained each sample with it's own unique hashing antibody so that we could subsequently pool the samples for loading onto the 10x Chromium and later prepare one library consisting of all sight samples and finally separate each sample in silico by it's unique hashing antibody. The samples are as follows: (1) HTO1: brain of naïve CCR2+/- mouse; (2) HTO2: brain of naïve CCR2+/- mouse; (3) HTO3: brain of naïve CCR2-/- mouse; (4) HTO4: brain of naive CCR2-/-; (5) HTO5: blood of naïve Cx3cr1+/- mouse; (6) HTO6: blood of metastasis-burdened Cx3cr1+/- mouse; (7) HTO7: blood of naïve Cx3cr1-/- mouse; (8) HTO8: blood of metastasis-burdened Cx3cr1-/- mouse.The following sample comparisons were made: HTO1 and HTO2 versus HTO3 and HTO4; HTO5 versus HTO7; HTO6 versus HTO8.

ORGANISM(S): Mus musculus

PROVIDER: GSE139969 | GEO | 2020/10/29

REPOSITORIES: GEO

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CNS-Native Myeloid Cells Drive Immune Suppression in the Brain Metastatic Niche through Cxcl10 [R07_Cx3cr1]

Project description:We performed CITE-seq (10x Genomics-based) to profile and compare the transcriptomes and cell surface expression of immune epitopes in the brains of Cx3cr1+/- and Cx3cr1-/- mice during homeostasis or brain metastasis. We sequenced a total of eight different samples. We created an antibody pool consisting of 35 different antibodies and stained each sample individually with this antibody pool. Then, we stained each sample with it's own unique hashing antibody so that we could subsequently pool the samples for loading onto the 10x Chromium and later prepare one library consisting of all sight samples and finally separate each sample in silico by it's unique hashing antibody. The samples are as follows: (1) HTO1: brain of naïve Cx3cr1+/- mouse; (2) HTO2: brain of naïve Cx3cr1+/- mouse; (3) HTO3: brain of metastasis-burdened Cx3cr1+/- mouse; (4) HTO4: brain of metastasis-burdened Cx3cr1+/- mouse; (5) HTO5: brain of naïve Cx3cr1-/- mouse; (6) HTO6: brain of naïve Cx3cr1-/- mouse; (7) HTO7: brain of metastasis-burdened Cx3cr1-/- mouse; (8) HTO8: brain of metastasis-burdened Cx3cr1-/- mouse. The following sample comparisons were made: HTO1 and HTO2 versus HTO5 and HTO6; HTO3 and HTO4 versus HTO7 and HTO8.

2020-10-29 | GSE139970 | GEO

CNS-Native Myeloid Cells Drive Immune Suppression in the Brain Metastatic Niche through Cxcl10 [R08_MgliaDep]

Project description:We performed CITE-seq (10x Genomics-based) to profile and compare the transcriptomes and cell surface expression of immune epitopes in the brains and blood of different transgenic mice (Cx3cr1CreERT; Cx3cr1CreERT-ROSA-iDTR) during homeostasis or brain metastasis with or without DT-based microglia depletion. We sequenced a total of eight different samples. We created an antibody pool consisting of 35 different antibodies and stained each sample individually with this antibody pool. Then, we stained each sample with it's own unique hashing antibody so that we could subsequently pool the samples for loading onto the 10x Chromium and later prepare one library consisting of all sight samples and finally separate each sample in silico by it's unique hashing antibody. The samples are as follows: (1) HTO1: brain of naïve Cx3cr1CreERT mouse (non-microglia depleted); (2) HTO2: brain of metastasis-burdened Cx3cr1CreERT mouse (non-microglia depleted); (3) HTO3: brain of metastasis-burdened Cx3cr1CreERT mouse (non-microglia depleted); (4) HTO4: brain of naïve Cx3cr1CreERT-ROSA-iDTR mouse (microglia depleted); (5) HTO5: brain of metastasis-burdened Cx3cr1CreERT-ROSA-iDTR mouse (microglia depleted); (6) HTO6: brain of metastasis-burdened Cx3cr1CreERT-ROSA-iDTR mouse (microglia depleted); (7) HTO7: blood of metastasis-burdened Cx3cr1CreERT mouse (non-microglia depleted); (8) HTO8: blood of metastasis-burdened Cx3cr1CreERT-ROSA-iDTR mouse (microglia depleted). The following sample comparisons were made: HTO1 versus HTO4; HTO2 and HTO3 versus HTO5 and HTO6; HTO7 versus HTO8.

2020-10-29 | GSE139971 | GEO

Chemotherapy-mediated changes in the immune cell landscape of murine triple negative breast cancer.

Project description:We performed CITE-seq (10x Genomics-based) to profile and compare the transcriptomes and cell surface expression of immune epitopes in the primary breast tumors of transgenic mice (C3-1-TAg) with or without MCT chemotherapy. We sequenced a total of six different tumor samples. We created an antibody pool consisting of 35 different antibodies and stained each sample individually with this antibody pool. Then, we stained each sample with it's own unique hashing antibody so that we could subsequently pool the samples for loading onto the 10x Chromium and later prepare one library consisting of all sight samples and finally separate each sample in silico by it's unique hashing antibody. The samples are as follows: (1) HTO1: tumor of PBS treated C3-1-TAg mouse; (2) HTO2: tumor of PBS treated C3-1-TAg mouse; (3) HTO3: tumor of PBS treated C3-1-TAg mouse; (4) HTO4: tumor of MCT treated C3-1-TAg mouse; (5) HTO5: tumor of MCT treated C3-1-TAg mouse; (6) HTO6: tumor of MCT treated C3-1-TAg mouse. The following sample comparisons were made: HTO1, HTO2, and HTO3 versus HTO4, HTO5, and HTO6.

2023-02-26 | GSE158888 | GEO

CNS-Native Myeloid Cells Drive Immune Suppression in the Brain Metastatic Niche through Cxcl10 [R10_PD-L1+VISTA treatment]

Project description:We performed CITE-seq (10x Genomics-based) to profile and compare the transcriptomes and cell surface expression of immune epitopes in the brains of anti-VISTA+anti-PD-L1 treated (Dual TX) and control, non-treated mice. We sequenced a total of eight samples (4 control, 4 dual TX). We created an antibody pool consisting of 35 different antibodies and stained each sample individually with this antibody pool. Then, we stained each sample with it's own unique hashing antibody so that we could subsequently pool the samples for loading onto the 10x Chromium and later prepare one library consisting of all sight samples and finally separate each sample in silico by it's unique hashing antibody. The samples are as follows: (1) HTO1: Control/Non-treated (2) HTO2: Control/Non-treated ; (3) HTO3: Control/Non-treated ; (4) Control/Non-treated ; (5) HTO5: Dual TX; (6) Dual TX; (7) HTO7: Dual TX; (8) HTO8: Dual TX. The following sample comparisons were made: HTO1 - HTO4 were compared to HTO5 - HTO8.

2020-10-29 | GSE158579 | GEO

A Spatially-Defined Metastasis-Associated Microglia Subset Promotes Brain Metastasis Outgrowth through Cx3cr1-Mediated Interferon Response

Project description:We use single cell RNA-seqencing (Drop-seq based) to profile and compare (1) the transcriptomes of naïve brain myeloid cells from wild type C57Bl/6 mice to brain metastasis-associated myeloid cells (Br.MAM) from C57Bl/6 mice bearing E0771 brain metastases and (2) the transcriptomes of Br.MAM in Cx3cr1+/- (het) mouse hosts bearing E0771 brain metastases to Br.MAM in Cx3cr1-/- (KO) mouse hosts bearing E0771 brain metastases.

2021-08-21 | GSE119229 | GEO

DNA methylome and transcriptome sequencing to define pathways involved in the activation of microglia

Project description:Microglia cells are macrophages which reside in the brain, and become activated during the inflammatory processes involved in neurodegenerative and autoimmune disorders. An understanding of the molecular processes involved in this activation process could lead to the development of new neuroprotective therapies. To reveal molecular mechanisms involved in microglia activation, we performed RNA-seq and MBD-isolated genome sequencing (MiGS or MBD-seq) on both naïve and peak microglia derived from the mouse experimental autoimmune encephalomyelitis (EAE) model. The EAE model reflects some of the histological and immunological features of multiple sclerosis (MS) in humans. Mice genetically engineered to label Ccr2 with red fluorescent protein (rfp) and Cx3cr1 with green fluorescent protein (gfp) (“red-green mice” as described in Saederup et al., 2010 and Mizutani et al., 2012) were employed and microglia (positive for gfp) were separated from infiltrating monocytes using flow cytometry.

2022-12-01 | GSE84424 | GEO

Cx3cr1 controls kidney resident macrophage heterogeneity

Project description:Kidney macrophages are comprised of both monocyte-derived and tissue resident populations; however, the heterogeneity of kidney macrophages and factors that regulate their heterogeneity are poorly understood. Herein, we performed single cell RNA sequencing (scRNAseq), fate mapping, and parabiosis to define the cellular heterogeneity of kidney macrophages in healthy mice. Our data indicate that healthy mouse kidneys contain four major subsets of monocytes and two major subsets of kidney resident macrophages (KRM) including a population with enriched Ccr2 expression, suggesting monocyte origin. Surprisingly, fate mapping data using the newly developed Ms4a3Cre Rosa Stopf/f TdT model indicate that less than 50% of Ccr2+ KRM are derived from Ly6chi monocytes. Instead, we find that Ccr2 expression in KRM reflects their spatial distribution as this cell population is almost exclusively found in the kidney cortex. We also identified Cx3cr1 as a gene that governs cortex specific accumulation of Ccr2+ KRM and show that loss of Ccr2+ KRM reduces the severity of cystic kidney disease in a mouse model where cysts are mainly localized to the kidney cortex. Collectively, our data indicate that Cx3cr1 regulates KRM heterogeneity and niche-specific disease progression.

2023-05-01 | GSE193892 | GEO

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Project description:We describe a novel subset of CD8+ DCs in lymphoid organs of naïve mice characterized by expression of the CX3CR1 chemokine receptor. CX3CR1+CD8+ DCs lack hallmarks of classical CD8+ DCs, including IL12 secretion, the capacity to cross-present antigen and their developmental independence of the transcriptional factor BatF3. Gene expression profiling showed that CX3CR1+CD8+ DCs resemble CD8- cDCs. The microarray analysis further revealed a unique plasmacytoid DC (PDC) gene signature of CX3CR1+ CD8+ DCs. A PDC relationship of the cells is further supported by the fact that they harbor characteristic D-J immunoglobulin gene rearrangements and that development of CX3CR1+CD8+ DCs requires E2-2, the critical transcriptional regulator of PDCs. Thus, CX3CR1+ CD8+ DCs represent a unique DC subset, related to but distinct from PDCs. After collagenase D digestion, spleens from Cx3cr1gfp/+ C57BL/6 mice were enriched for CD11c+ cells by magnetic separation according to the manufacturer’s protocol (MiltenyiBiotec GmbH). Splenic CD11chi cells were isolated using the FACS ARIA high-speed sorter (Becton-Dickinson). Total RNA was extracted and subjected to gene expression profiling using the Mouse Genome 430.2 Affymetrix GeneChip

2010-07-28 | E-GEOD-23212 | biostudies-arrayexpress

Mononuclear phagocytes in muscle after notexin injury in C57Bl/6, Cx3cr1-/-, Ccl2-/-,Cx3cr1-/-Ccl2-/- mice

Project description:Muscle injury triggers inflammation in which infiltrating mononuclear phagocytes are crucial for tissue regeneration. The interaction of the CCL2/CCR2 and CX3CL1/CX3CR1 chemokine axis that guides phagocyte infiltration is incompletely understood. Here, we show that CX3CR1 deficiency promotes muscle repair and rescues Ccl2-/- mice from impaired muscle regeneration as a result of altered macrophage function, not infiltration. Transcriptomic analysis of muscle mononuclear phagocytes reveals that Apolipoprotein E (ApoE) is up-regulated in mice with efficient regeneration. ApoE treatment enhances phagocytosis by mononuclear phagocytes in vitro, and restores phagocytic activity and muscle regeneration in Ccl2-/- mice. Because CX3CR1 deficiency may compensate for defective CCL2-dependant monocyte recruitment by modulating ApoE-dependent macrophage phagocytic activity, targeting CX3CR1 expressed by macrophages might be a powerful therapeutic approach to improve muscle regeneration.

2015-09-29 | GSE73473 | GEO

Inhibition of Intimal CX3CR1+ Macrophages Mitigates Thoracic Aortic Aneurysm Progression in Marfan Syndrome

Project description:Current understanding on the pathogenesis of thoracic aortic aneurysms (TAAs) in Marfan Syndrome (MFS) mainly focuses on vascular smooth muscle cell (VSMC) pathologies. Whether immune cell-mediated inflammation drives the progression of TAAs is still elusive. Using single-cell RNA sequencing, a subset of macrophages highly expressing CX3CR1 and mainly locating in the aortic intima was identified in aortic root and ascending aortas from Fbn1C1041G/+ mice, and further validated in MFS patients. Specific elimination of CX3CR1+ macrophages by diphtheria toxin in Cx3cr1-CreERT2iDTRF/+Fbn1C1041G/+ mice efficiently ameliorated TAA progression, suggesting their pathogenic action. Using monoclonal antibodies Adalimumab and Teprotumumab to respectively neutralize the proinflammatory cytokines TNFalpha and IGF1 produced by CX3CR1+ macrophages from MFS patients substantially suppressed CX3CR1+ macrophage-mediated inflammation in MFS patient-specific induced pluripotent stem cell (iPSC)-derived VSMCs. Furthermore, bone marrow transplantation and parabiosis using Cx3cr1GFP/+ mice revealed the intimal CX3CR1+ macrophages derived from circulating monocytes. Administration of CCR2 antagonist RS504393 to inhibit monocyte infiltration significantly reduced intimal CX3CR1+ macrophages and subsequently alleviated TAA development in Fbn1C1041G/+ mice. In conclusion, intimal CX3CR1+ macrophages mediated TAA formation through paracrinally causing VSMC inflammation. Targeting intimal CX3CR1+ macrophages would be a promising anti-inflammatory strategy in TAA therapy for MFS.

2024-12-10 | GSE249352 | GEO

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