High glucose-induced human cellular immune response is governed by miR-2909 RNomics.

Regulation of NFkB family member RelA translocation by tumour suppressor genes encoding p53 and KLF4, has been widely recognized as the critical for human peripheral blood mononuclear cells (PBMCs) to meet their energy requirement for tailoring their immune response against any perceived threat. Our study was addressed to understand as to how human PBMCs respond to high glucose threat in terms of their genomics-directed immune response. The results of such a study revealed for the first time that NFkB induced miR-2909 RNomics is crucial for the regulation of RelA translocation within human PBMCs exposed to high glucose thereby enabling these epigenetically programmed cells to tailor immune response involving genes coding for CCL5; IFN-γ and IL-17. Based upon these results an attempt was also made to propose a mechanistic pathway that links high glucose induced cellular miR-2909 RNomics with the genes involved in energy metabolism and immune response.