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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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The glomerular mRNA expression data from podocyte specific GC-A and p38MAPK double knockout mice

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

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Deep RNA Sequencing of native mouse podocytes and non-podocytes glomerular cells

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2019-01-01 | E-MTAB-5457 | biostudies-arrayexpress

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

Project description:Innate immune checkpoint has emerging as a highly potential target for cancer immunotherapy in recent years. The CD47-SIRPα axis is the best-studied innate checkpoint in cancer. However, the transcription profile of tumor cell duiring CD47-SIRPα blockade therapy remains unclear.

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Tumor cell intrinsic type I interferon signaling dictates CD47-SIRPα blockade immunotherapy via metabolic reprograming [dataset 2]

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2015-11-24 | E-GEOD-66969 | biostudies-arrayexpress

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