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1. Identification of critical residues of linear B cell epitope on Goodpasture autoantigen.

Author

Xiao-yu Jia, Zhao Cui, Jian-nan Li, Shui-yi Hu, and Ming-hui Zhao

Subjects
Medicine, Science
Abstract

BACKGROUND:The autoantigen of anti-glomerular basement membrane (GBM) disease has been identified as the non-collagenous domain 1 of α3 chain of type IV collagen, α3(IV)NC1. Our previous study revealed a peptide on α3(IV)NC1 as a major linear epitope for B cells and potentially nephrogenic, designated as P14 (α3129-150). This peptide has also been proven to be the epitope of auto-reactive T cells in anti-GBM patients. This study was aimed to further characterize the critical motif of P14. METHODS:16 patients with anti-GBM disease and positive anti-P14 antibodies were enrolled. A set of truncated and alanine substituted peptides derived from P14 were synthesized. Circulating antibodies against the peptides were detected by enzyme linked immunosorbent assay (ELISA). RESULTS:We found that all sera with anti-P14 antibodies reacted with the 13-mer sequence in the C-terminus of P14 (P14c) exclusively. The level of antibodies against P14 was highly correlated with the level of antibodies against P14c (r=0.970, P

Published
2015
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2. The alternative pathway of complement activation may be involved in the renal damage of human anti-glomerular basement membrane disease.

Author

Rui Ma, Zhao Cui, Shui-Yi Hu, Xiao-Yu Jia, Rui Yang, Xin Zheng, Jie Ao, Gang Liu, Yun-Hua Liao, and Ming-Hui Zhao

Subjects
Medicine, Science
Abstract

Linear deposition of IgG and complement 3 (C3) along glomerular basement membrane (GBM) is generally revealed in the kidneys of human anti-GBM disease. Our recent studies demonstrated the pathogenic role of complement activation in renal damage of this disease. However, the pathways of complement activation were still paradoxical. In this study, renal biopsy tissues from 10 patients with anti-GBM disease were used to investigate the pathways of complement activation by detecting the deposition of various complement components, including C1q, factor B, factor P (properdin), mannose-binding lectin (MBL), C3d, C4d and C5b-9, using immunohistochemistry and immunofluorescence. We found that C1q, factor B, properdin, C3d, C4d and C5b-9 were detected in all the glomeruli of our patients, along GBM with a linear and/or granular staining pattern. Furthermore, C1q, factor B and properdin co-localized well with C5b-9. The properdin also co-localized well with C3d. However, the deposition of MBL was diffusive in mesangium, GBM, Bowman's capsule and within crescents and was not co-localized with C5b-9 but partially co-localized with C4d. The intensity of factor B deposition (3.3 vs. 1.2, P

Published
2014
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3. Plasma from patients with anti-glomerular basement membrane disease could recognize microbial peptides

Author

Can Xie, Zhao Cui, Yongqiang Wang, Ming-Hui Zhao, Taijiao Jiang, Jian-nan Li, and Xiao-yu Jia

Subjects
0301 basic medicine, Male, Anti-Glomerular Basement Membrane Disease, Physiology, 030232 urology & nephrology, lcsh:Medicine, Peptide, medicine.disease_cause, Severity of Illness Index, Biochemistry, Immunoglobulin G, Database and Informatics Methods, 0302 clinical medicine, Aromatic Amino Acids, Immune Physiology, Medicine and Health Sciences, Bacteroides, Enzyme-Linked Immunoassays, Amino Acids, Database Searching, lcsh:Science, Databases, Protein, Peptide sequence, chemistry.chemical_classification, Multidisciplinary, Immune System Proteins, biology, Organic Compounds, Chemical Synthesis, Acute Kidney Injury, Middle Aged, Molecular mimicry, Chemistry, Creatinine, Physical Sciences, Female, Antibody, Sequence Analysis, Research Article, Adult, Vasculitis, Genotype, Biosynthetic Techniques, Bioinformatics, Phenylalanine, Immunology, Saccharomyces cerevisiae, Research and Analysis Methods, Antibodies, Antibodies, Antineutrophil Cytoplasmic, 03 medical and health sciences, Sequence Motif Analysis, medicine, Humans, Amino Acid Sequence, Immunoassays, Peptide Synthesis, Molecular Biology, Autoantibodies, lcsh:R, Molecular Mimicry, Organic Chemistry, Autoantibody, Chemical Compounds, Biology and Life Sciences, Proteins, biology.organism_classification, 030104 developmental biology, chemistry, Immunoglobulin M, biology.protein, Immunologic Techniques, lcsh:Q, Bifidobacterium, Peptides, HLA-DRB1 Chains
Abstract

Infection has long been suspected as a trigger of autoimmune diseases, and molecular mimicry mechanism was hypothesized in this study. Microbe originated peptides were searched from the Uniprot database based on a previous defined critical amino acid motif within α3129-150, isoleucine137, tryptophan140, glycine142, phenylalanine 143 and phenylalanine 145. 23826 microbial peptides were identified using our searching strategy, among which seven were related with human infections. Circulating IgG and IgM antibodies against the seven microbial peptides were detected using ELISA in 76 patients with anti-GBM disease. Four peptides were recognized by both IgG and IgM antibodies, and one peptide was recognized by IgG antibodies only. Peptides from Bacteroides, Saccharomyces cerevisiae, and Bifidobacterium thermophilum possessed the highest recognition frequency with the prevalence of 73.7%, 61.8% and 67.1% for IgG, 56.6%, 44.7% and 67.1% for IgM in anti-GBM patients. Patients with antibodies against these microbial peptides showed more severe kidney injury, including higher serum creatinine and higher percentage of crescent formation. In conclusion, antibodies against microbial peptides were identified in the circulation of anti-GBM patients, implying its etiological role in eliciting autoimmune response against α3(IV)NC1 through molecular mimicry.

Published
2016

4. The Alternative Pathway of Complement Activation May Be Involved in the Renal Damage of Human Anti-Glomerular Basement Membrane Disease

Author

Xiao-yu Jia, Gang Liu, Shui-yi Hu, Rui Ma, Jie Ao, Rui Yang, Ming-Hui Zhao, Zhao Cui, Xin Zheng, and Yunhua Liao

Subjects
Male, Pathology, Physiology, Anti-Glomerular Basement Membrane Disease, Complement System, lcsh:Medicine, Fluorescent Antibody Technique, urologic and male genital diseases, Kidney, Biochemistry, Basement Membrane, Cell Signaling, Endocrine Signaling, Immune Physiology, Molecular Cell Biology, Chronic Kidney Disease, Medicine and Health Sciences, lcsh:Science, Complement Activation, Multidisciplinary, Immune System Proteins, Glomerular basement membrane, Complement C3, Middle Aged, female genital diseases and pregnancy complications, Extracellular Matrix, medicine.anatomical_structure, Mesangium, Nephrology, Female, Anatomy, Cellular Structures and Organelles, Research Article, Signal Transduction, Adult, medicine.medical_specialty, Immunology, chemical and pharmacologic phenomena, Endocrine System, Biology, Complement factor B, Classical complement pathway, medicine, Humans, Aged, urogenital system, lcsh:R, Biology and Life Sciences, Proteins, Renal System, Cell Biology, Complement system, Immune System, Immunoglobulin G, Alternative complement pathway, Properdin, lcsh:Q, Clinical Immunology
Abstract

Linear deposition of IgG and complement 3 (C3) along glomerular basement membrane (GBM) is generally revealed in the kidneys of human anti-GBM disease. Our recent studies demonstrated the pathogenic role of complement activation in renal damage of this disease. However, the pathways of complement activation were still paradoxical. In this study, renal biopsy tissues from 10 patients with anti-GBM disease were used to investigate the pathways of complement activation by detecting the deposition of various complement components, including C1q, factor B, factor P (properdin), mannose-binding lectin (MBL), C3d, C4d and C5b-9, using immunohistochemistry and immunofluorescence. We found that C1q, factor B, properdin, C3d, C4d and C5b-9 were detected in all the glomeruli of our patients, along GBM with a linear and/or granular staining pattern. Furthermore, C1q, factor B and properdin co-localized well with C5b-9. The properdin also co-localized well with C3d. However, the deposition of MBL was diffusive in mesangium, GBM, Bowman's capsule and within crescents and was not co-localized with C5b-9 but partially co-localized with C4d. The intensity of factor B deposition (3.3 vs. 1.2, P

Published
2014

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