2026-10-13T04:28:25Z https://www.scidb.cn/oai

10.57760/sciencedb.j00217.13474 2026-06-01T15:07:30Z

2026-06-01 From Immunosenescence to Immune Resetting: Research Advances in the Pathogenesis of Systemic Lupus Erythematosus and Clinical Translation Strategies doi:10.57760/sciencedb.j00217.13474 en Systemic lupus erythematosus (SLE), as the most heterogeneous autoimmune disease, has traditionally been viewed as being caused by autoantibody-mediated immune complex deposition and excessive activation of the classical complement pathway. Research over the past five years has revealed more complex mechanisms: T cell immunosenescence, non-classical functions of the complement lectin pathway, the crosstalk between autophagy and PANoptosis, and the concept of "molecular refractoriness" — all of which are reshaping the understanding of SLE. Therapeutic strategies are shifting from "broad-spectrum immunosuppression" toward "immune homeostasis reconstruction" and "immune system resetting", including low-dose IL-2, JAK inhibitors, and CAR-T cell therapy. Centered on the theme "from immunosenescence to immune resetting", this article integrates cutting-edge advances, proposes a patient stratification framework based on molecular pathway mapping, and aims to promote individualized precision therapy. Systemic lupus erythematosus; Immunosenescence; Molecular refractoriness; Low-dose interleukin-2; JAK inhibitors; CAR-T cell therapy Yuanli.Shan Xiaopu.Shen Jiazhuo.Li Juan.Du PUBLIC https://creativecommons.org/publicdomain/zero/1.0/ dataset Science Data Bank