Metabolomics,Unknown,Transcriptomics,Genomics,Proteomics

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Expression data of CD4+T cells from Idiopathic CD4+ T cells lymphopenia (ICL) patients, Sarcoidosis (SARC) and Healthy individuals


ABSTRACT: This work focuses on understanding the molecular basis of the immune dysfunctions in Idiopathic CD4+ T cells lymphocytopenia (ICL). ICL is a rare haematological disorder of unknown origin, characterized by a profound and persistent CD4+ T-cell defect, which predisposes to life threatening opportunistic infections very similar to those seen in AIDS. To analyse more in depth the functional pathways involved in ICL pathogenesis, we conducted gene expression profiling of CD4+ T-cells isolated from blood samples from ICL, sarcoidosis and healthy individuals. Our analyses have revealed specific CD4+ T-cells gene expression signatures in ICL associated with defective TCR activation threshold, expansion of the Treg-cell compartment and interestingly with accelerated immune aging. 25 Total samples were analyzed. We generated the following pairwise comparisons using GenoSplice technology. We permormed multiple anlayses including : ICL vs Healthy (All or paired samples), ICL vs SARC (All or paired samples) and SARC vs Healthy (All or paired sample). Paired samples means that a same healthy individual was using in comparaison of a ICL or SARC subjects. Genes with a Fold-change ? 1,5 and P-Value ? 0,05 were selected.

ORGANISM(S): Homo sapiens

SUBMITTER: Pierre de la Grange 

PROVIDER: E-GEOD-56998 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Idiopathic CD4 lymphopenia (ICL) is a rare heterogeneous immunological syndrome of unclear etiology. ICL predisposes patients to severe opportunistic infections and frequently leads to poor vaccination effectiveness. Chronic immune activation, expansion of memory T cells, and impaired T-cell receptor (TCR) signaling have been reported in ICL, but the mechanistic and causative links remain unclear. We show that late-differentiated T cells in 20 patients with ICL displayed defective TCR responses  ...[more]

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