Oral Abstract
Therapeutic Apheresis
Ning Li (he/him/his)
Director
Department of Blood Transfusion, Xiangya Hospital, NHC Key Laboratory of Cancer Proteomics, Central South University, Changsha, Hunan Province, China
changsha, Hunan
Disclosure information not submitted.
Systemic lupus erythematosus (SLE) remains a therapeutic challenge due to its heterogeneous immune dysregulation and limited efficacy of conventional therapies. While therapeutic plasmapheresis has been explored for severe SLE, its efficacy remains controversial. Evidences implicating lymphocytes and RBCs retaining mitochondria in disease pathogenesis. Given that lymphoplasmapheresis (LPE) effectively depletes lymphocytes and whole-blood exchange (WBE) removes whole blood, including pathogenic RBCs, the blood exchange transfusion (BET) combining of LPE and WBE may represent a promising alternative to current second-line therapies for refractory SLE. This study aims to evaluate the efficacy and safety of BET in SLE.
Study
Design/Methods:
This retrospective study evaluated the efficacy and immunomodulatory mechanisms of BET on SLE, including 84 severe SLE patients unresponsive to glucocorticoids/immunosuppressants underwent BET (BET group) and 61 controls receiving conventional therapy (CT group). Systemic Lupus Erythematosus Disease Activity Index (SLEDAI) scores, proteinuria, glucocorticoid requirements, C3, C4, CRP, hematologic parameters, immunologic profiles and longitudinal follow-up were analyzed. Flow cytometry and ELISA were conducted to delineate the regulation of BET on T-cell subtypes and cytokines.
Results/Findings:
BET exhibited marked efficacy in attenuating SLE disease manifestations, as evidenced by significant improvements in urinary protein, C3, C4, CRP, and SLEDAI (from16.5±1.4 to 15.1±1.2, p< 0.01), alongside a reduction in serum immunoglobulins, including IgA, IgM, IgG and glucocorticoid requirements (from 103.8± 14.0 to 62.1±8.0 mg/d, p<a name="OLE_LINK5"> < 0.001). In contrast, CT showed no significant impact on proteinuria, IgA, IgM and CRP levels, nor did it alter glucocorticoid dosing (Figure a). In both AIHA and immune thrombocytopenia (ITP) subgroup, BET not only elevated Hb and PLT levels but also suppressed anti-IgG and anti-C3 of anti-human globulin test (Figure b). Flow cytometry revealed BET-mediated rebalancing of T-cell subsets, marked by expanded regulatory T cells (p < 0.05) and reduced Th17 frequencies, alongside diminished proinflammatory cytokines (IL-17A, TNF-α, p< 0.05) and elevated anti-inflammatory mediators (IL-10, TGF-β1) (Figure c). Longitudinal follow-up demonstrated sustained benefits, including reduced proteinuria at 12 months and neutrophil driven inflammation at 3 months (Figure d). BET targets both humoral and cellular immune dysregulation by removing pathogenic autoantibodies, lymphocytes and erythrocytes.
Conclusions:
These findings position BET as a multifaceted intervention capable of rapidly controlling disease flares and mitigating organ damage in refractory SLE. The study underscores the therapeutic potential of BET in recalibrating immune homeostasis, offering a novel strategy to bridge the gap between conventional therapies and biologic agents in SLE management.