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The dysfunctions of complement factor H in lupus nephritis
1Renal Division, Department of Medicine, Peking University First Hospital; Institute of Nephrology, Peking University, PR China Key Laboratory of Renal Disease, Ministry of Health of China, PR China; Key Laboratory of CKD Prevention and Treatment, Ministry of Education of China, PR China Institute of Nephrology, Zhongda Hospital, Southeast University, Nanjing, PR China.
Lupus
|April 13, 2016
Summary
Factor H (FH) dysfunction in lupus nephritis patients impairs complement regulation and apoptotic cell clearance. These functional deficits are linked to specific FH genetic variations (SNPs) and clinical symptoms.
Area of Science:
- Immunology
- Nephrology
- Genetics
Background:
- Previous studies indicated decreased plasma Factor H (FH) levels in lupus nephritis patients, correlating with disease activity.
- This study investigates the in vitro biofunctions of plasma FH in lupus nephritis.
Purpose of the Study:
- To analyze the in vitro biofunctions of purified plasma Factor H (FH) from lupus nephritis patients.
- To explore the potential association between FH genetic variations and its impaired functions.
Main Methods:
- Purification of FH from plasma of lupus nephritis patients, systemic lupus erythematosus (SLE) patients, and healthy controls.
- In vitro assays to assess FH binding capabilities (C3b, mCRP), erythrocyte lysis protection, and apoptotic cell phagocytosis induction.
- Exome sequencing analysis of FH in lupus nephritis patients.
Main Results:
- Purified FH from lupus nephritis patients showed significantly reduced abilities in C3b/mCRP binding and erythrocyte protection compared to controls.
- FH from lupus nephritis patients demonstrated impaired induction of late apoptotic cell phagocytosis.
- Identified single nucleotide polymorphisms (SNPs) in FH exons (rs1061147, rs1061170, CM050194, CM010322) in all lupus nephritis patients studied.
Conclusions:
- Factor H (FH) exhibits functional dysregulation in some active lupus nephritis patients, affecting complement alternative pathway regulation and apoptotic cell clearance.
- These FH dysfunctions correlate with patient clinical phenotypes.
- Identified FH single nucleotide polymorphisms (SNPs) may contribute to the observed functional impairments in lupus nephritis.
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