Introduction: Celiac disease (CeD) is an autoimmune condition characterized by a reversible inflammatory reaction in the mucous membrane of the small intestine. Nevertheless, there is a limited availability of efficient control approaches. Prior research has demonstrated that pharmacological targets supported by genetic evidence can greatly enhance the efficacy of drug development. Hence, the study aims to integrate transcriptomic and proteomic information to identify candidate targets for CeD. Methods: The study employed proteome-wide Mendelian randomization (MR) analysis of circulating plasma proteins to investigate their causal association with CeD. The candidate targets for CeD were further assessed employing colocalization analysis, transcriptome-wide summary-data-based Mendelian randomization (SMR) analysis, multimarker analysis of genomic annotation (MAGMA) gene-based analysis, and bulk RNAseq-based differential expression analysis. For the proteins that were identified, extended Phenome-wide association studies (PheWAS) were conducted to assess their side-effect profiles, while the DGIdb database provided information on the approved or investigated drugs for candidate targets. Results: Systematic MR analysis identified 22 candidate targets for CeD. Among the proteins analyzed, BTN2A1 passed all subsequent verification analyses. Additionally, three proteins, including CatH, IL-18R1, and PTPRC, passed the majority of the subsequent verification analyses. The other 18 proteins were also candidate targets (Trehalase, CD226, SH2B3, ICOSLG, ULK3, Park7, ALDH2, RABEP1, TNFRSF9, COL11A2, GNPDA1, IL-1RL1, B3galt6, TNFSF11, CCL21, BTN3A3, OLFM2 and Colipase). Conclusions: The study employed a combination of human transcriptomic and proteomic information, employing several analytical methods. As a result, 22 proteins, divided into four tiers, were identified as prospective therapeutic targets for CeD.