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Table 1_RNA therapeutics in rheumatoid arthritis, systemic lupus erythematosus, and systemic sclerosis: a compartment-aware translational framework.docx Yusif Afandizada (25311768) Hikmet Memmedov (25311771) Mushfig Orujov (25311774) Shahla Eyvazova (25311777) Shirkhan Amikishiyev (23951823) Genetic Immunology antisense oligonucleotides drug delivery lupus nephritis rheumatoid arthritis RNA therapeutics small interfering RNA systemic lupus erythematosus systemic sclerosis <p>Rheumatoid arthritis (RA), systemic lupus erythematosus/lupus nephritis (SLE/LN), and systemic sclerosis (SSc) remain major causes of chronic inflammation, disability, organ damage, and treatment burden despite therapeutic advances. RNA therapeutics offer programmable transcript suppression, network-level microRNA modulation, transient restoration of protective proteins, and targeting-ligand functions. Existing reviews largely catalogue modalities or individual delivery systems; this review instead asks whether a candidate forms an interpretable translational program across target biology, disease compartment, intended cell, productive intracellular access, direct target engagement, pathway pharmacodynamics, repeat-dose safety, and manufacturing feasibility. RA is primarily a synovial immune–stromal delivery problem in which RNA programs must also demonstrate an advantage over effective biologic or targeted synthetic therapies. SLE/LN offers interferon, B-cell, co-stimulatory, microRNA, messenger RNA (mRNA), and complement opportunities, but therapeutic nucleic acids and carriers must not intensify nucleic-acid sensing, interferon activity, or complement-associated injury. SSc combines strong antifibrotic RNA biology with an accessible skin proof-of-mechanism window, whereas lung, vascular, and internal-organ programs remain more delivery-limited. We separate human pathway validation, RNA-platform evidence outside the target disease, disease-specific RNA evidence, and patient efficacy. Recent human complement-factor-B pharmacodynamic data strengthen the platform-level evidence but do not establish efficacy in RA or LN. The most informative early trials will therefore be biomarker-enriched and mechanism-rich, with prespecified criteria that distinguish target failure from delivery, dose, endotype, or safety failure.</p> 2026-10-05T12:07:53Z Dataset Dataset 10.3389/fimmu.2026.1950465.s001 https://figshare.com/articles/dataset/Table_1_RNA_therapeutics_in_rheumatoid_arthritis_systemic_lupus_erythematosus_and_systemic_sclerosis_a_compartment-aware_translational_framework_docx/34069560 CC BY 4.0