Abstract
Background: The leukaemia-derived Jurkat E6.1 cell line has been used as a model T cell in the study of many aspects of T cell biology, most notably activation in response to T cell receptor (TCR) engagement. Methods: We present whole-transcriptome RNA-Sequencing data for Jurkat E6.1 cells in the resting state and two hours post-activation via TCR and CD28. We compare early transcriptional responses in the presence and absence of the chemokines CXCL12 and CCL19, and perform a basic comparison between observed transcriptional responses in Jurkat E6.1 cells and those in primary human T cells using publicly deposited data. Results: Jurkat E6.1 cells have many of the hallmarks of standard T cell transcriptional responses to activation, but lack most of the depth of responses in primary cells. Conclusions: These data indicate that Jurkat E6.1 cells hence represent only a highly simplified model of early T cell transcriptional responses.
Highlights
Adaptive immunity is centred on the clonal selection and activation of lymphocytes, most importantly T cells, which provide stimulation and regulation to other cells of the immune system as well as directly killing infected cells
Jurkat responses broadly correspond to expected effects of T cell activation and are unaffected by the presence of chemokines RNA-Seq was performed on total mRNA collected from Jurkat E6.1 cells under both resting and activated conditions (total mapped counted given in Extended data - Dataset S1 (Felce, 2020b))
The Jurkat E6.1 cell line has been extensively used as a model of T cell biology, in the study of T cell receptor (TCR) signalling
Summary
Adaptive immunity is centred on the clonal selection and activation of lymphocytes, most importantly T cells, which provide stimulation and regulation to other cells of the immune system as well as directly killing infected cells. T cells become activated in response to binding of their clonally specific T cell receptors (TCRs) to cognate peptide-major histocompatibility complexes (pMHCs) on the surface of interacting antigenpresenting cells. This leads to recruitment and phosphorylation of a series of kinases and adaptor proteins to the TCR, intracellular Ca2+ mobilisation, and consequent downstream changes in gene expression – largely due to activation of nuclear factor of activated T cells (NFAT) – which mark the transition to a fully activated state. The leukaemia-derived Jurkat E6.1 cell line has been used as a model T cell in the study of many aspects of T cell biology, most notably activation in response to T cell receptor (TCR) engagement. Conclusions: These data indicate that Jurkat E6.1 cells represent only a highly simplified model of early T cell transcriptional responses.
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