Early T helper cell programming of gene expression in human

Abstract

Molecular mechanisms guiding naïve T helper cell differentiation into functionally specified effector cells are intensively studied. The rapidly growing knowledge is mainly achieved by using mouse cells or disease models. Comparatively exiguous data is gathered from human primary cells although they provide the "ultimate model" for immunology in man, have been exploited in many original studies paving the way for the field, and can be analyzed more easily than ever with the help of modern technology and methods. As usage of mouse models is unavoidable in translational research, parallel human and mouse studies should be performed to assure the relevancy of the hypothesis created during the basic research. In this review, we give an overview on the status of the studies conducted with human primary cells aiming at elucidating the mechanisms instructing the priming of T helper cell subtypes. The special emphasis is given to the recent high-throughput studies. In addition, by comparing the human and mouse studies we intend to point out the regulatory mechanisms and questions which are lacking examination with human primary cells.

Keywords: ChIA-PET; ChIP; ChIP-seq; Epigenetics; Genome-wide; High-throughput; Human; RNA interference; RNA-seq; RNAi; SNP; STAT; T cell receptor; T helper cell; TCR; Tfh; Th; Transcription; UTR; chromatin immunoprecipitation; chromatin immunoprecipitation coupled to high-throughput sequencing; chromatin interaction analysis by paired-end tag sequencing; follicular T helper cell; high-throughput RNA sequencing; iTreg; inducible T regulatory cell, adaptive T regulatory; lincRNA; lncRNA; long intergenic non-coding RNA; long non-coding RNA; miRNA; microRNA; short interfering RNA; siRNA; signal transducer and activator of transcription; single nucleotide polymorphism; untranslated region of mRNA.