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Background <p>The complement system critically mediates systemic lupus erythematosus (SLE) pathogenesis through dual mechanisms: promoting inflammatory organ damage while regulating the initiation of immune tolerance. Among its three activation pathways (classical, alternative, and lectin), the lectin pathway is the most recently characterized.</p> Findings <p>The lectin pathway engages pattern-recognition molecules (PRMs: mannose-binding lectin [MBL], collectins, ficolins) and mannose-binding lectin–associated serine proteases (MASPs). These components orchestrate unique biological functions beyond canonical complement activation, including self-antigen clearance, B/T-cell tolerance modulation, and interferon-α production. PRM/MASP genetic variants (particularly loss-of-function genotypes) predispose to SLE and associate with organ-specific damage phenotypes. PRMs detect damage-associated molecular patterns on apoptotic cells, initiating complement activation. Resulting fragments (C3a, C5a) and membrane attack complexes directly drive tissue injury. Clinically, circulating PRM/MASP levels and tissue deposition patterns reflect disease activity and organ involvement. Although MASP-2- and C5-targeting monoclonal antibodies demonstrate therapeutic potential in trials, most lectin pathway interventions remain preclinical.</p> Conclusions <p>This review integrates clinical correlations, mechanistic advances in both complement-dependent and complement-independent functions, and emerging SLE therapeutics targeting the lectin pathway.</p>

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Advances in the lectin pathway in systemic lupus erythematosus: from clinical correlations and mechanisms to targeted interventions

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2026年2月26日

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  • Rongfang Feng,
  • Yufei Zhang,
  • Qin Chen,
  • Yaqi Wang,
  • Yaning Tian,
  • Yumin Xia

摘要

Background

The complement system critically mediates systemic lupus erythematosus (SLE) pathogenesis through dual mechanisms: promoting inflammatory organ damage while regulating the initiation of immune tolerance. Among its three activation pathways (classical, alternative, and lectin), the lectin pathway is the most recently characterized.

Findings

The lectin pathway engages pattern-recognition molecules (PRMs: mannose-binding lectin [MBL], collectins, ficolins) and mannose-binding lectin–associated serine proteases (MASPs). These components orchestrate unique biological functions beyond canonical complement activation, including self-antigen clearance, B/T-cell tolerance modulation, and interferon-α production. PRM/MASP genetic variants (particularly loss-of-function genotypes) predispose to SLE and associate with organ-specific damage phenotypes. PRMs detect damage-associated molecular patterns on apoptotic cells, initiating complement activation. Resulting fragments (C3a, C5a) and membrane attack complexes directly drive tissue injury. Clinically, circulating PRM/MASP levels and tissue deposition patterns reflect disease activity and organ involvement. Although MASP-2- and C5-targeting monoclonal antibodies demonstrate therapeutic potential in trials, most lectin pathway interventions remain preclinical.

Conclusions

This review integrates clinical correlations, mechanistic advances in both complement-dependent and complement-independent functions, and emerging SLE therapeutics targeting the lectin pathway.