To discover new rheumatoid arthritis (RA) risk loci, we systematically examined 370 SNPs from 179 independent loci with P < 0.001 in a published meta-analysis of RA genome-wide association studies (GWAS) of 3,393 cases and 12,462 controls. We used Gene Relationships Across Implicated Loci (GRAIL), a computational method that applies statistical text mining to PubMed abstracts, to score these 179 loci for functional relationships to genes in 16 established RA disease loci^,,,,,,,,,. We identified 22 loci with a significant degree of functional connectivity. We genotyped 22 representative SNPs in an independent set of 7,957 cases and 11,958 matched controls. Three were convincingly validated: CD2-CD58 (rs11586238, P = 1 × 10⁻⁶ replication, P = 1 × 10⁻⁹ overall), CD28 (rs1980422, P = 5 × 10⁻⁶ replication, P = 1 × 10⁻⁹ overall) and PRDM1 (rs548234, P = 1 × 10⁻⁵ replication, P = 2 × 10⁻⁸ overall). An additional four were replicated (P < 0.0023): TAGAP (rs394581, P = 0.0002 replication, P = 4 × 10⁻⁷ overall), PTPRC (rs10919563, P = 0.0003 replication, P = 7 × 10⁻⁷ overall), TRAF6-RAG1 (rs540386, P = 0.0008 replication, P = 4 × 10⁻⁶ overall) and FCGR2A (rs12746613, P = 0.0022 replication, P = 2 × 10⁻⁵ overall). Many of these loci are also associated to other immunologic diseases.