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BCR repertoire analysis by Next-generation sequencing of lymphocytes harvested from mice vaccinated with liposomal TLR4 and TLR7 agonists

ABSTRACT: BCR repertoire analysis by Next-generation sequencing of lymphocytes harvested from mice vaccinated with liposomal TLR4 and TLR7 agonists

PROVIDER: PRJEB37157 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	ERR3981360_1.fastq.gz	Fastqsanger.gz
	ERR3981360_2.fastq.gz	Fastqsanger.gz
	ERR3981370_1.fastq.gz	Fastqsanger.gz
	ERR3981370_2.fastq.gz	Fastqsanger.gz
	ERR3981380_1.fastq.gz	Fastqsanger.gz

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BCR repertoire analysis by Next-generation sequencing of lymphocytes harvested from mice vaccinated with liposomal TLR4 and TLR7 agonists

Project description:BALB/c mice were vaccinated with inactivated influenza A virus adjuvanted with liposomal TLR4 (2B182C) and TLR7 agonists (2B182C) on days 0 and 21. To examine whether the liposomal combined adjuvant increase BCR diversity, lymphocytes in the draining lymph nodes harvested on day 28 were analyzed using next-generation RNA sequencing technology.

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Treatment of human monocytes with TLR7 or TLR8 agonists

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Project description:Endosomal Toll-like receptors (TLRs) play an important role in the etiology of systemic autoimmune diseases such as SLE, where DNA- and RNA-associated autoantigens activate autoreactive B cells through TLR9- and TLR7-dependent pathways, respectively. Nevertheless, TLR9-deficient autoimmune prone mice develop more severe clinical disease, while TLR7-deficient and TLR7/9-double deficient autoimmune-prone mice develop less severe disease. To determine whether the regulatory activity of TLR9 is B cell intrinsic, we have now directly compared the functional properties of autoantigen activated WT, TLR9-deficient and TLR7-deficient B cells, in an experimental system where proliferation depends on BCR/TLR co-engagement. In vitro, TLR9-deficient cells are less dependent on survival factors for a sustained proliferative response than either WT or TLR7-deficient cells. The TLR9-deficient cells also preferentially differentiate toward the plasma cell lineage, as indicated by expression of CD138, sustained expression of IRF4, and other molecular markers of plasma cells. In vivo, autoantigen-activated TLR9-deficient cells give rise to greater numbers of autoantibody producing cells. Our results identify distinct roles for TLR7 and TLR9 in the differentiation of autoreactive B cells that explain the capacity of TLR9 to limit, and TLR7 to promote, the clinical features of SLE. AM14 WT, Tlr7-/-, Tlr9-/- and Tlr7/9-/- B cells were stimulated with PL2-3 for 0, 6, 24, and 42 hours, for a total of 16 samples.

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