| Issue |
BIO Web Conf.
Volume 237, 2026
2026 8th International Conference on Biotechnology and Biomedicine (ICBB 2026)
|
|
|---|---|---|
| Article Number | 01016 | |
| Number of page(s) | 6 | |
| Section | Molecular and Cellular Pathophysiology | |
| DOI | https://doi.org/10.1051/bioconf/202623701016 | |
| Published online | 10 June 2026 | |
Review in the Recent Advances in Host Immune Molecules and Autoimmune Diseases
American International School of Budapest, Budapest, 2094, Hungary
* Corresponding author: This email address is being protected from spambots. You need JavaScript enabled to view it.
Abstract
Host immune molecules—e.g. cytokines, chemokines, complement factors, antibodies, and regulatory checkpoints—illustrate duality by protecting the body against pathogens yet driving autoimmune pathology when dysregulated. This review focuses on five axes: innate nucleic acid recognition, inflammatory cytokine networks, humoral-complement immunity, immune regulation and checkpoints as well as chemokine-tissue microenvironments. Together, these systems illustrate how dose, timing, and context cooperatively determine the bodily immune status and outcome. Key molecular markers, including BAFF/APRIL, IL-6, IFN-I, IL-17/IL-23, and C5a exemplify the “double-edged sword” nature of immune signaling: their excess or deficiency contributes respectively to diseases such as systemic lupus erythematosus, rheumatoid arthritis, psoriasis, and vasculitis. Therapies targeting these molecules demonstrate the viability of precision immunotherapy, and future research comprising of multi-omics profiling and spatiotemporal immune analysis may refine biomarker-guided treatment and enable context-specific modulation, hence helping to achieve balanced immune intervention in autoimmune diseases.
© The Authors, published by EDP Sciences, 2026
This is an Open Access article distributed under the terms of the Creative Commons Attribution License 4.0, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
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