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Transcript profiling of WT and SIRPα KO BMDMs post-M1 activation in the presence of mCD47.ex

ABSTRACT: Transcript profiling of WT and SIRPα KO BMDMs post-M1 activation in the presence of mCD47.ex

PROVIDER: PRJNA715480 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR14001646.fastq.gz	Fastqsanger.gz
	SRR14001647.fastq.gz	Fastqsanger.gz

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Transcript profiling of WT and SIRPα KO BMDMs post-M1 activation in the presence of mCD47.ex

Project description:To compare the inflammatory responses of WT and SIRPα KO macrophage, we performed a complete transcript profiling of WT and SIRPα-KO M1 macrophage using transcriptome sequencing as a discovery platform. SIRPα-KO mice and WT mice were kept under the same condition. BMDMs were produced from WT and SIRPα-KO mice followed by M1 polarization. RNA was then isolated from the same number of BMDMs.

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N-terminal pyroglutamate in CD47 is involved in SIRPα interactions

Project description:T-cell immune checkpoint inhibitors have revolutionized cancer immunotherapy. In addition to T cells, immune checkpoint molecules have also been described for myeloid cells, with CD47 on tumor cells and Signal Regulatory Protein α (SIRPα) on effector cells being the most established example (Maute et al. Immunooncol Technol. 2022). Blockade of this checkpoint by CD47 or SIRPα targeting molecules has been demonstrated to enhance the efficacy of therapeutic antibodies in many preclinical tumor models (Müller et al. Blood. 2022, Schewe et al. Hemasphere. 2024). Next to CD47/SIRPα blocking molecules, inhibition of Glutaminyl-Peptide Cyclotransferase-Like (QPCTL) - the enzyme that catalyzes functionally relevant pyroglutamate (pGlu) formation on many peptides and proteins including CD47 - was shown to modify the myeloid tumor cell infiltrate (Barreira et al. Nat Immunol. 2022) and to improve antibody-dependent cellular phagocytosis (ADCP) and antibody-dependent cellular cytotoxicity (ADCC) against tumor cells (Logtenberg et al. Nat Med. 2019, Wu et al. Cell Res. 2019, Baumann et al. Front Immunol. 2021). Crystallographic analyses of CD47 in complex with SIRPα revealed that the CD47 binding pocket for SIRPα contains pGlu at the N-terminus (Hatherley et al. Mol Cell. 2008). However, on cellular level the direct involvement of pGlu in the CD47/SIRPα interaction has not been confirmed yet. We generated human CD47 Fc proteins, that contain either a native CD47 ectodomain with N-terminal pGlu (CD47-wt) or a mutated version with alanine at the N-terminus (CD47-Q1A), which was confirmed by mass spectrometry. Differential binding of CD47-wt and CD47-Q1A revealed that pGlu on CD47 is essential for binding to SIRPα on macrophages, supporting that inhibition of QPCTL is a good therapeutic option for enhanced tumor cell killing through CD47/SIRPα interference.

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Project description:Type-2 innate lymphoid cells (ILC2) are part of a growing family of innate lymphocytes known for their crucial role in both the development and exacerbation of allergic asthma. In this study, we aim to elucidate the critical role of the suppressor molecule signal regulatory protein alpha (SIRPα), which interacts with CD47, in controlling ILC2-mediated airway hyperreactivity (AHR). Our data indicate that activated ILC2s upregulate the expression of SIRPα, and the interaction between SIRPα and CD47 effectively suppresses both ILC2 proliferation and effector function. To evaluate the efficacy of SIRPα in regulating ILC2-mediated AHR, we utilized SIRPα and CD47 deficient mice in a murine model of allergen-induced AHR. Our findings suggest that the absence of SIRPα leads to the overactivation of ILC2s. Conversely, engagement with SIRPα reduces ILC2 cytokine production and effectively regulates ILC2-dependent AHR. Furthermore, the SIRPα-CD47 axis modulates mitochondrial metabolism through the JAK/STAT and ERK/MAPK signaling pathways, thereby regulating NF-κB activity and the production of type two cytokines. Additionally, our studies on human cells have revealed that SIRPα is inducible and expressed on human ILC2s, and administration of a SIRPα agonist effectively suppresses the effector function and cytokine production of ILC2s. Moreover, administering human CD47-Fc to humanized ILC2 mice effectively alleviated AHR and lung inflammation. These findings highlight the promising therapeutic potential of targeting the SIRPα-CD47 axis in the treatment of ILC2-dependent allergic asthma.

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Project description:Purpose: The purpose of this study was to compare the BMDMs transcriptome in the control LPS and LPS plus BHB group in order to identify the critical pathway that contributed to the inhibiton of BHB on M1 polarization. Methods: 1× 106 BMDMs were pre-treated with PBS or BHB for 1 hours before LPS administration. Four hours later, BMDMs were harvested for RNA preparation. Results: Among 16650 mapped genes, 7325 differentially expressed genes were identified, including 244 LPS inducible BHB down regulated named class A and 537 LPS repressed BHB up regulated genes named class B. The genes in class A were mainly TLR4 and TNF signaling pathway, while genes in class B were associated with negative regulation of transcription and NF-KB signaling. The GSEA showed that BHB have the similar profiles chnage on BMDMs with TSA. Conclusions: Our study revealed that BHB down regulated TLR4 and NF-KB pathway related genes to inhibited M1 polarization, and BHB have a similar effect on BMDMs with TSA through comparing the genetic changes of two substance caused in cells.

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Project description:Signal regulatory protein α (SIRPα) is a well-characterized inhibitory receptor expressed on myeloid immune cells. We and others have recently discovered that human and mouse melanoma cells express high levels of SIRPα. However, whether and how melanoma-intrinsic SIRPα contributes to tumor progression and anti-tumor immunity remains underexplored. Here, we identify a novel role of tumor-intrinsic SIRPα in suppressing anti-tumor immune recruitment and activation. Genetic deletion of SIRPα in melanoma cells enhanced tumor control and increased infiltration of immune cells into the tumor. Transcriptomic analysis revealed that loss of melanoma cell-intrinsic SIRPα leads to upregulation of C-X-C motif chemokine 10 (CXCL10) expression in both human and mouse melanoma cells. Notably, knockdown of Cxcl10 in SIRPα-deficient melanoma cells partially rescued tumor growth and reduced CD8+ T cell infiltration, recapitulating the phenotype observed in SIRPα-expressing tumors. These findings indicate that tumor cell-intrinsic SIRPα suppresses anti-tumor immunity by inhibiting Cxcl10 expression, thereby compromising T cell recruitment to the tumor sites. Thus, our work uncovers a previously unrecognized mechanism by which melanoma cell-intrinsic SIRPα suppresses anti-tumor immunity and highlights the therapeutic potential of silencing SIRPα to enhance anti-tumor immune cell infiltration and promote T cell-mediated tumor control. We envision that SIRPα silencing as a therapeutic strategy that could be applied to other cancer types that express SIRPα.

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