English: Modular and pathway analysis reveal a dominant IFN-inducible signature in tuberculosis. Modular analysis reveals overabundance of IFN-inducible genes (M3.1) and myeloid genes (M1.5 and M2.6) and under abundance of B (M1.3) and T cell (M2.8) related genes (A) (4); (B) (From Cliff et al., Distinct phases of blood gene expression pattern through tuberculosis treatment reflect modulation of the humoral immune response. J Infect Dis 2013; 207(1): pp. 18–29, by permission of Oxford University Press). (12). (C) The canonical pathway for IFN signaling from Ingenuity Pathways Analysis; with transcripts over-represented in test set patients with active tuberculosis (1, 4) shaded red. GAS, Gamma-activated site; ISRE, IFN-sensitive element. Modified from (1, 4). Transcript abundance in whole blood and (c) separated blood leucocyte populations of representative IFN-inducible genes (from top to bottom: OAS1, IFI6, IFI44, IFI44L, OAS3, IRF7,IFIH1, IFI16, IFIT3, IFIT2, OAS2, IFITM3, IFITM1, GBP1, GBP5, STAT1, GBP2, TAP1, STAT1, STAT2, IFI35, TAP2, CD274, SOCS1, CXCL10, IFIT5) in active tuberculosis. Transcript abundance/expression is normalized to the median of the healthy controls. Modified from (A and C modified from Berry et al., Nature 2010) (1, 3, 4).