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Finally, we report both ancestry-dependent and ancestry-independent contributions to SLE risk. In total, 27,574 SLE cases and controls from three ancestral groups were genotyped and passed quality control for the Immunochip (AA: 2,970 cases, 2,452 controls; EA: 6,748 cases, 11,516 controls; HA: 1,872 cases and 2,016 controls). Table 1 shows the number of distinct regions (see Methods) within each ancestry that reached three tiers of statistical significance (Tier 1: PManhattan plots for (a) European ancestry, (b) African American, (c) Hispanic ancestry, and the (d) meta-analysis. Systemic lupus erythematosus (SLE) is an autoimmune disease with marked gender and ethnic disparities. We report a large transancestral association study of SLE using Immunochip genotype data from 27,574 individuals of European (EA), African (AA) and Hispanic Amerindian (HA) ancestry. The 8p11 (PLAT) association is novel to SLE and was not observed in HA or EA as it was nearly monomorphic in both populations.

These 58 regions include 24 novel SLE regions reaching genome-wide significance (P).

Many are novel SLE risk regions, and others are novel for EA (Table 2).

More than 50% of these regions had multiple independent SNPs contributing to the association, based on regional stepwise analyses.

Altogether, 146,111 SNPs passed quality control analyses in at least one ancestry (AA: 128,385, EA: 120,873, HA: 120,786). Tier 1 associations are labelled with novel regions highlighted in red.

Restricting linkage disequilibrium (LD) to r=1.13 (Supplementary Fig. Genome-wide significance (5 × 10Statistically, EA had the most power and 58 regions met Tier 1 or Tier 2 thresholds (Supplementary Data 2).

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