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Expression of CD39 and CD45RO on CD4+CD25hi T cells identifies human naïve (G3) and effector Treg (G2), and distinguishes them from activated non-Treg cells (Tresp).

ABSTRACT: Human responder T-cells (Tresp) and 2 lineages of regulatory T cells (Tregs), namely G2 and G3, were isolated by flow sorting based on their immunoreacitivities against specific cell surface markers and their gene expression profiles were interrogated using Affymetrix Exon 1.0 ST Arrays

ORGANISM(S): Homo sapiens

PROVIDER: GSE47667 | GEO | 2013/10/01

SECONDARY ACCESSION(S): PRJNA207083

REPOSITORIES: GEO

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Project description:Neuroblastoma (NB) is an aggressive tumor that affects both infants and children. The disease outcome is greatly influenced by age of patient, stage, chromosome copy number aberrations (CNAs) and gene expression abnormalities. We analyzed, by microarray technology, genome and transcriptome of 3 groups of tumors of patients with metastatic disease: G1, stage 4S and MYCN single copy; G2, stage 4 younger than 18 months of age, MYCN single copy with no disease progression and G3, stage 4, older than 19 months, with unfavorable outcome. We found an accumulation of structural copy number aberrations (CNAs) in G3 whereas G1 tumors had mostly numerical (N) CNAs and G2 showed an intermediate behavior. Pair wise comparisons demonstrated that the average of N CNAs significantly decreased from G1 to G2 to G3 (9.6 G1 < 7.2 G2 < 3.6 G3); in contrast S CNAs significantly increased in G3 (0.7 G1 < 3.7 G2 < 7.0 G3). Interestingly, we observed several intra-chromosomal rearrangements in G3 tumors on chromosomes not usually involved in NB. Excluding MYCN amplified tumors by G3 we found a high frequency of S CNAs in this group. Gene expression analysis showed a deregulation of downstream genes of Ras and Rho signaling pathway among the 3 groups. It has been also observed a progressive switch off of development and adhesion genes and a switch on of cell cycle genes from G1 to G2 to G3. Moreover, the telemorase genes were significantly expressed in G3 with respect to remaining groups. Present data show an accumulation of S CNAs from stage 4S to 4. The deregulation of genes Rho/Ras pathway may explain the increase of tumor aggressiveness from G1 to G2 to G3. The increase of cell cycle and telomerase genes expression associated with G3 would provide unlimited replicative potential for these tumors and may be responsible for accumulation of S CNAs. Finally, we can argue that accumulation of structural aberrations and gene deregulation is age-dependent and it is associated with a more aggressive tumor phenotype.

Dataset Information

Expression of CD39 and CD45RO on CD4+CD25hi T cells identifies human naïve (G3) and effector Treg (G2), and distinguishes them from activated non-Treg cells (Tresp).

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