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Data · dataset · 2026

From Immunosenescence to Immune Resetting: Research Advances in the Pathogenesis of Systemic Lupus Erythematosus and Clinical Translation Strategies

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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.

Description

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.

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Catalogue records · 1

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Inferred from text
Disease 75%
Provenance · 1 source records, 11 field assertions
SourceKeyLast seenRaw
ScienceDB10.57760/sciencedb.j00217.1347410 d agoJSON v1
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