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Loss of SIRPα promotes podocytes presenting antigen to activate specific T cell immune responses in lupus nephritis via activating spleen tyrosine kinase

ABSTRACT: To investigate the role of SIRPα in podocytes, we generated podocyte-specific SIRPα knockout mice, Subsequent studies have found that SIRPa is deeply involved in the adaptive immune process of podocytes, and the loss of SIRPa promotes the ability of podocytes to present antigens,furthermore, the loss of SIRPa in podocytes can promote the increase of antigen presentation ability of podocytes and promote the progression of lupus nephrin

ORGANISM(S): Mus musculus

PROVIDER: GSE240916 | GEO | 2024/05/24

REPOSITORIES: GEO

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Loss of SIRPα promotes podocytes presenting antigen to activate specific T cell immune responses in lupus nephritis via activating spleen tyrosine kinase

Project description:Loss of SIRPα promotes podocytes presenting antigen to activate specific T cell immune responses in lupus nephritis via activating spleen tyrosine kinase

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SIRPα-CD47 axis regulates ILC2 effector function and alleviates airway hyperreactivity via modulating energy metabolism.

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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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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Project description:Purpose: Next-generation sequencing (NGS) was used to define the transcriptome of native mouse podocytes and non-podocytes glomerular cells as part of a project aiming to define the molecular fingerprint of mouse podocytes. Method: Glomeruli from 29 Gt(ROSA)26Sortm4(ACTB-tdTomato,-EGFP)Luo/J x hNPHS2Cre mice at the age of 10 weeks were purified and a single cell solution was prepared to seperate GFP-expressing (podocytes) and GFP-negative (non-podocytes glomerular cells) cells by FACS sorting. RNA was extracted and prepared for further analysis using directional, polyA+ library preparation. An Illumina HiSeq2500 was used for a paired-end sequencing of 100 cycles . Salmon and Sleuth were used for downstream analysis. Results: A total of 100 Million reads each from podocytes and non-podocytes glomerular cells could be used for further analysis.

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Gene expression profiling of human iPS cell-derived podocytes and sorted human adult podocytes

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Tumor cell intrinsic type I interferon signaling dictates CD47-SIRPα blockade immunotherapy via metabolic reprograming [dataset 1]

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Differentiation of human amniotic fluid kidney progenitor cells into podocytes and comparison with human conditionally immortalized podocytes

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