Activation of Transposable Elements in Immune Cells of Fibromyalgia Patients

Figures

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  Figure 1. HERVs are overexpressed in FM. RT-qPCR amplification of HERV-H, HERV-K and HERV-W using total RNA from PBMCs is shown (N = 14/group) (*** p < 0.001; *p < 0.05). Primer sets are detailed in Table 2 and conditions used described in Methods. Relative expression levels were calculated as 2−ΔΔCt values using GAPDH levels as reference. Group means and SEM values are shown.

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  Figure 2. INF-β and INF-γ levels are increased and TNF-α are unaffected in FM patients showing increased HERV levels. RT-qPCR amplification of INF-β and INF-γ and TNF-α are shown (N = 14/group); (*** p < 0.001; ** p < 0.005); ns (non-significant). Primers sets used are detailed in Table 2 and conditions described in Methods. Relative expression was calculated as 2−ΔΔCt values using GAPDH levels as reference. Group means and SEM values are shown.

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  Figure 3. Linear regression analysis of HERV-H, HERV-K and HERV-W levels with respect to INF-β (A–C) and INF-γ (D–F) levels in PBMCs of FM patients. Adjusted calculated best-fit lines together with SD values (dotted lines) are represented for each data set pair; R2 and p values are indicated.

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  Figure 4. Linear regression analysis of HERV-H, HERV-K and HERV-W levels with respect to each other (A–C); and correlation between INF-β and INF-γ levels (D) in PBMCs of FM patients are shown. Adjusted calculated best-fit lines together with SD values (dotted lines) are represented for each data set pair; R2 and p values are indicated.

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  Figure 5. Northern blot analysis of tRNA levels in PBMCs from FM or HC participants, as indicated (A). Quantitated tRNA-His, tRNA-Pro levels (Image J software) upon normalization to RNU6 levels are shown (B) (N = 4/group).

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  Figure 6. Proposed mechanism linking overexpression of HERVs, INF induction and increased cancer susceptibility in patients with defective ribonuclease activity. ISF (Interferon stimulating factors); TLR3 (Toll-like receptor 3); MDA5 (Melanoma differentiation associated gene 5); RIG-I (Retinoic acid-inducible gene I); OAS (2’-5’-oligoadenylate synthetase); 2-5A (2’, 5’ oligomers of ATP); tsRNAs (transfer RNA small fragments); RT (reverse transcription); AGO (Argonaut).