Review highlights immune molecules’ roles in diseases and implications for precision immunotherapy.
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.
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Kexin Zhou (2026) studied this question.
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