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Next Generation Sequencing for Quantitative Transcriptomic Profiling of TLR3 and TLR7 activation in Bone-marrow-derived macrophage

ABSTRACT: Next Generation Sequencing for Quantitative Transcriptomic Profiling of TLR3 and TLR7 activation in Bone-marrow-derived macrophage

PROVIDER: PRJNA685788 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR13260212.fastq.gz	Fastqsanger.gz
	SRR13260213.fastq.gz	Fastqsanger.gz
	SRR13260214.fastq.gz	Fastqsanger.gz
	SRR13260215.fastq.gz	Fastqsanger.gz
	SRR13260216.fastq.gz	Fastqsanger.gz

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Next Generation Sequencing for Quantitative Transcriptomic Profiling of TLR3 and TLR7 activation in Bone-marrow-derived macrophage

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UNC93B1 variants underlie TLR7-dependent autoimmunity

Project description:UNC93B1 is critical for trafficking and function of nucleic acid-sensing Toll-like receptors (TLRs) TLR3, TLR7, TLR8, and TLR9, which are essential for antiviral immunity. Overactive TLR7 signaling induced by recognition of self-nucleic acids has been implicated in systemic lupus erythematosus (SLE). Here, we report UNC93B1 variants (E92G and R336L) in four patients with early-onset SLE. Patient cells or mouse macrophages carrying the UNC93B1 variants produced high amounts of TNF-α and IL-6 and upon stimulation with TLR7/TLR8 agonist, but not with TLR3 or TLR9 agonists. E92G causes UNC93B1 protein instability and reduced interaction with TLR7, leading to selective TLR7 hyperactivation with constitutive type I IFN signaling. Thus, UNC93B1 regulates TLR subtype-specific mechanisms of ligand recognition. Our findings establish a pivotal role for UNC93B1 in TLR7-dependent autoimmunity and highlight the therapeutic potential of targeting TLR7 in SLE.

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