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
The Ox40/Ox40 Ligand Pathway Promotes Pathogenic Th Cell Responses, Plasmablast Accumulation, and Lupus Nephritis in NZB/W F1 Mice.
Cell line, Treatment, Subject
View SamplesWe''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 promotes disease. To that end we performed RNASeq on in vitro cultured CD4 T cells during Ox40 and TCR stimulation (in a reductionist setting) to understand how Ox40 signaling impacts cellular phenotype and function, including with and without TCR stimulation Overall design: RNASeq was performed on in vitro cultured CD4 T cells from the spleen of NZB/W F1 lupus prone mice, following anti-Ox40 mAb and anti-CD3/CD28 bead stimulation
The Ox40/Ox40 Ligand Pathway Promotes Pathogenic Th Cell Responses, Plasmablast Accumulation, and Lupus Nephritis in NZB/W F1 Mice.
Cell line, Subject
View Samples