ArrayExpress Uploader0mouseC57BL/6, Tissue: Spleen, Mouse number: pooled cells from 10 miceC57BL/6, Tissue: Sacral and pancreatic lymph node, Mouse number: pooled cells from 20 miceC57BL/6, Tissue: Spleen, Mouse number: pooled cells from 10 miceC57BL/6, Tissue: Spleen, Mouse number: pooled cells from 10 miceC57BL/6, Tissue: Spleen, Mouse number: pooled cells from 10 miceC57BL/6, Tissue: Sacral and pancreatic lymph node, Mouse number: pooled cells from 20 miceC57BL/6, Tissue: Spleen, Mouse number: pooled cells from 10 mice5618arrayexpress_sid6Peripheral tolerance induction is critical for the maintenance of self-tolerance and can be mediated by immunoregulatory T cells or by...19204323E-GEOD-14699/profile/8773/arrayexpressuploader17cellil-7rlymphopeniaperipheralproteinDec.12, 2014FalseE-GEOD-14699_A-AFFY-45expression-data-from-cd8-t-cells-undergoing-deletiExpression data from CD8+ T cells undergoing deletional toleranceNov.10, 2014Peripheral tolerance induction is critical for the maintenance of self-tolerance and can be mediated by immunoregulatory T cells or by direct induction of T cell anergy or deletion. While the molecular processes underlying anergy have been extensively studied, little is known about the molecular basis for peripheral T cell deletion. Here, we determined the gene expression signature of peripheral CD8+ T cells undergoing deletional tolerance, relative to those undergoing immunogenic priming or lymphopenia-induced proliferation. From these data, we report the first detailed molecular signature of cells undergoing deletion. Consistent with defective cytolysis, these cells exhibited deficiencies in granzyme up-regulation. Furthermore, they showed antigen-driven Bcl-2 down-regulation and early up-regulation of the pro-apoptotic protein Bim, consistent with the requirement of this BH3-only protein for peripheral T cell deletion. Bim up-regulation was paralleled by defective IL-7Ra chain re-expression, suggesting that Bim-dependent death may be triggered by loss of IL-7/IL-7R signaling. Finally, we observed parallels in molecular signatures between deletion and anergy suggesting that these tolerance pathways may not be as molecularly distinct as previously surmised. Naïve (CD44lo) OT-I T cells were CFSE labelled and transferred in a model of deletional tolerance (RIP-OVAhi mice), a model of immunity (mice primed with OVA coated splenocytes and LPS) or a model of lymphopenia induced proliferation (Rag-/- mice). 60 hrs (RIP-OVAhi and OVA coated splenocytes) or 5 days (Rag-/-) after transfer, OT-I cells that had undergone two or more divisions as determined by CFSE dilution were sorted, RNA extracted and samples were prepared for hybridisation to Affymetrix microarrays. As a control for naive cells, CFSE labelled OT-I cells were injected into antigen-free B6 mice and the undivided naive cells were sorted after 60 hrs and also used for microarray analysis. Two replicates were prepared for the naive cells, cells from RIP-OVAhi mice and cells from OVA coated splenocyte primed mice, while one replicate was prepared for the cells from Rag-/- mice.http://www.ebi.ac.uk/arrayexpress/experiments/E-GEOD-14699http://www.ebi.ac.uk/arrayexpress/experiments/E-GEOD-14699/samples/