Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2026
Advances in the lectin pathway in systemic lupus erythematosus: from clinical correlations and mechanisms to targeted interventions.
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Feng Rongfang, Zhang Yufei, Chen Qin, Wang Yaqi, Tian Yaning, Xia Yumin
Аннотация
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.
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.