Figure 3. Replication and expansion of APS1 autoantigens across multiple cohorts using scaled phage-immunoprecipitation sequencing (PhIP-seq).

(A) Increasing the number of healthy controls results in fewer apparent hits and is therefore critical. Shared hits are defined as gene-level signal (>10-fold change over mock-IP) which is shared among 4%< of APS1 samples (n=128), present in fewer than 2% of healthy controls, and with at least one APS1 sample with a high signal (FC of 50<). Random downsampling was performed 10 times for each healthy control bin. (B) 39 candidate hits present in 4%< of the APS1 cohort. (C) Rare, novel anti-PDYN autoantibodies validate at whole-protein level, with PhIP-seq and whole-protein RLBA data showing good concordance.