ReviewPharmaceutics2026
Therapeutic Applications of Immunobiologics in Autoimmune and Inflammatory Diseases.
Review in Pharmaceutics, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
0 citing papers in PubMed.
No citing paper in PubMed yet.
Corrections and comments
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Authors and funding
1 author.
Funding
Abstract
Immunobiologics or biologics have revolutionized the therapeutic paradigm of autoimmune and inflammatory diseases by selectively targeting and modulating dysregulated immune pathways. Compared with conventional broad-spectrum immunosuppressants, biologics provide a more specific and mechanism-based rational approach, often associated with improved efficacy and reduced adverse events. This review provides a comprehensive overview of the repertoire of therapeutic biologics, their mechanisms of action, pivotal clinical trials, and clinical applications. We discuss biologics targeting T-cell activation, depletion, and adhesion, as well as agents neutralizing pro-inflammatory cytokines, including tumor necrosis factor (TNF), interleukin (IL)-1, IL-6, IL-12, IL-17, IL-22, and IL-23, in addition to B-cell-directed therapies and IgE-modulating agents. Evidence from randomized clinical trials and observational studies highlights the profound therapeutic impact of these agents across a broad spectrum of immune-mediated diseases, including rheumatoid arthritis, psoriasis, systemic lupus erythematosus (SLE), ankylosing spondylitis, chronic spontaneous urticaria, asthma, ulcerative colitis, Crohn's disease, and other forms of inflammatory bowel disease (IBD). Pharmacodynamic parameters, including receptor-binding affinity and downstream pathway modulation, are critical determinants of therapeutic efficacy, whereas pharmacovigilance remains indispensable for monitoring risks such as immunogenicity, opportunistic infections, and manufacturing-related variability. Continuous regulatory oversight by agencies such as the United States Food and Drug Administration (FDA) and the European Medicines Agency (EMA) safeguards standards of safety, efficacy, and quality. In parallel, the expanding development of biosimilars offers a key opportunity to enhance affordability and broaden global access to biologic therapies. Despite substantial clinical progress, important challenges persist, including disease heterogeneity, variability in therapeutic response, long-term safety concerns, and issues of cost-effectiveness. Future directions emphasize precision medicine strategies, including biomarker-guided treatment, rationally designed biologic combinations, next-generation antibody engineering, and the development of high-quality biosimilars to improve therapeutic durability, safety, and accessibility equity. By integrating mechanistic insights with clinical outcomes, this review underscores the transformative role of immunobiologics and delineates strategies to optimize their application in the management of autoimmune and inflammatory diseases.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.