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. Author manuscript; available in PMC: 2018 Mar 12.
Published in final edited form as: Sci Transl Med. 2017 Jul 12;9(398):eaal1243. doi: 10.1126/scitranslmed.aal1243

Fig. 3. Early induction of ZBTB7A in LTxRs who developed de novo DSA and BOS.

Fig. 3

BAL cell ZBTB7A expression was evaluated by quantitative PCR after normalization with ACTB, CD68, and PPARG (91). Delta Ct values at 3 months post-LTx were set as baseline for respective LTxRs (sTable 2), and relative expression for subsequent time points was calculated as 2−ΔΔCt. (A) ZBTB7A induction in a cohort of 21 BOS+ LTxRs and time-matched 21 LTxRs who remained BOS-free, (B) kinetic study at 6±1 and 12±1 post-LTx months on 12 LTxRs who later developed BOS and (C) 11 LTxRs who remained stable were evaluated. (D) Ten LTxRs who developed de novo DSA (MFI >2000) and received Ab-directed therapies were stratified as pre-DSA (MFI<2000), DSA-peaked (highest MFI observed during follow-up of individual patient), DSA-reduced (2000<MFI<Peak), and DSA-resolved (MFI<2000). (E) Serial samples from eight stable LTxRs (DSA− and not treated by Ab-directed therapies) were evaluated. (F) Role of DSA and autoAb (anti-Kα1T, anti-Col V) in ZBTB7A induction evaluated in LTxRs DSA−autoAb− (n=11); DSA−autoAb+ (either anti-Kα1T or anti-Col V, n=5); DSA+autoAb− (n=10); DSA+one autoAb (either anti-Kα1T or anti-Col V, n=11) and DSA+two autoAbs (anti-Kα1T and anti-Col V, n=19). Two-tailed Mann-Whitney U test was applied and p values are indicated. Significance of the results is marked at p<0.05 (*).