Fig 2: Redox stress markers and antioxidant responses upon HIV-1 infection in bulk and live primary CD4+ T cells ATime course of the protein expression of total and phosphorylated eIF2a in HIV-1-infected and mock-infected primary CD4+ T cells.B, C Nrf2 (B) and gag (C) mRNA expression in HIV-1-infected Jurkat-TAg cells transfected with non-targeting siRNA (NC) or siRNAs targeting the Nrf2 gene. Cells were infected 24 h post-transfection and assayed for mRNA expression by qPCR 48 h post-infection. Data (mean ± SEM; n = 4 technical replicates) were normalized using 18S as housekeeping gene and expressed as fold change in siRNA Nrf2-treated cells vs. NC control and analyzed by unpaired t-test.DRelative (infected vs. mock-infected) mRNA levels of main targets of Nrf2 during the transition from productive (3–9 dpi) to latent (14 dpi) infection.EEfficiency of magnetic enrichment of viable primary CD4+ T cells. Live cells were isolated by negative selection (Annexin V binding), stained with a LIVE/DEAD dye before and after enrichment, and analyzed by flow cytometry.FRelative (infected vs. mock-infected) mRNA levels of the targets analyzed in panel (D), performed on cells previously enriched for viability.GRelative mRNA expression of Nrf2 downstream antioxidant targets in Jurkat T cells left untreated or treated for 24 h with 10 µM TPA.Data information: Data in (F, G) were normalized using 18S, while data in (D) were normalized using GAPDH as housekeeping genes. After normalization, data were expressed log2 fold mRNA expression in infected vs. mock-infected (D, F) or untreated vs. TPA-treated cells (G) as in Livak and Schmittgen (2001). Data are shown as mean ± SEM of 3 biological replicates and were analyzed by two-way ANOVA followed by Tukey's post-test for multiple comparisons. *P < 0.05; **P < 0.01; ****P < 0.0001. Trx = thioredoxin; NQO1 = NAD(P)H [quinone] dehydrogenase 1; HMOX-1 = heme oxygenase 1; G6PD = glucose-6-phosphate dehydrogenase; GCLC = glutamate-cysteine ligase; TrxR1 = thioredoxin reductase 1.Source data are available online for this figure.

Fig 3: TrxR1 knockdown decreases BCR/NF-?B pathway-related mRNA and protein expression. SUDHL2 and SUDHL4 cells were transfected with TrxR1 specific siRNA (siTrxR) and a scrambled siRNA (control). (A,B), RT-qPCR was performed 48 h after transfection to determine the mRNA expression of TrxR1, BTK, p65, and surviving in SUDHL2 and SUDHL4 cells. (C,D), Western blotting was performed 48 h after transfection to determine the protein levels of BTK and TrxR in SUDHL2 and SUDHL4 cells. (E,F), The BTK expression was detected after treating cells with the indicated [Au(d2pype)2]Cl after 24 h in SUDHL2 and SUDHL4 cells. B-actin was used as the loading control for BTK protein blots, and Vinculin was used as the loading control for the TrxR protein blots. Western blots are representative of 3 independent experiments. Significance levels are marked as * p < 0.05 and ** p < 0.005.

Fig 4: Correlation analysis of expression of genes of the Trx system and BCR signalling pathway. Expression of TXNRD1, TXN, and PRDX1 in comparison with BTK, RelA, and XIAP expression in DLBCL (n = 48). (A–C), correlation analysis between BTK and TXNRD1 (A), TXN (B), and PRDX1 (C); (D–F), correlation analysis between RelA and TXNRD1 (D), TXN (E), and PRDX1 (F); (G–I), correlation analysis between XIAP and TXNRD1 (G), TXN (H), and PRDX1 (I). The correlation coefficient® was calculated using Spearman’s r correlation analysis, and p values are displayed.