Dataset Information


RNASeq to identify the in vivo mechanism of anti-Ox40 mAb treatment exacerbated lupus in NZB/W F1 Mice

ABSTRACT: We've recently shown that we can accelerate disease in a model of SLE (the NZB/W F1 model) using an anti-Ox40 mAb treatment regimen. The disease acceleration is rapid (within 2 weeks) but its unclear, mechanistically, how OX40 functions to promote disease. To that end we want to perform RNASeq on the sorted OX40-expressing CD4 T cells during treatment to understand how they function in response to OX40 signaling in vivo Overall design: RNASeq was performed on FACS sorted CD4 T cells from the spleen and kidney of NZB/W F1 lupus mice following anti-Ox40 agonist mAb treatment and disease acceleration

INSTRUMENT(S): Illumina HiSeq 2500 (Mus musculus)

SUBMITTER: Jonathan Sitrin 

PROVIDER: GSE99646 | GEO | 2017-08-18



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The Ox40/Ox40 Ligand Pathway Promotes Pathogenic Th Cell Responses, Plasmablast Accumulation, and Lupus Nephritis in NZB/W F1 Mice.

Sitrin Jonathan J   Suto Eric E   Wuster Arthur A   Eastham-Anderson Jeffrey J   Kim Jeong M JM   Austin Cary D CD   Lee Wyne P WP   Behrens Timothy W TW  

Journal of immunology (Baltimore, Md. : 1950) 20170710 4

Ox40 ligand (Ox40L) locus genetic variants are associated with the risk for systemic lupus erythematosus (SLE); however, it is unclear how Ox40L contributes to SLE pathogenesis. In this study, we evaluated the contribution of Ox40L and its cognate receptor, Ox40, using in vivo agonist and antagonist approaches in the NZB × NZW (NZB/W) F1 mouse model of SLE. Ox40 was highly expressed on several CD4 Th cell subsets in the spleen and kidney of diseased mice, and expression correlated with disease s  ...[more]

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