Analysis of serum-derived and internalized complement component C3 bound DNA sequences
Ontology highlight
ABSTRACT:
PROVIDER: PRJEB30321 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| ERR2992300_1.fastq.gz | Fastqsanger.gz | |||
| ERR2992300_2.fastq.gz | Fastqsanger.gz | |||
| ERR2992301_1.fastq.gz | Fastqsanger.gz | |||
| ERR2992301_2.fastq.gz | Fastqsanger.gz | |||
| ERR2992294_1.fastq.gz | Fastqsanger.gz |
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Project description:The most abundant and central component, glycoprotein C3, contributes to the development of type 1 diabetes by enhancing the organ-specific autoimmune inflammatory processes. It is known that changes in glycosylation can modulate inflammatory responses and we recently showed that children at the onset of type 1 diabetes have a higher proportion of oligomannose glycans in plasma N-glycome compared to their healthy siblings. Due to fact that C3 contains two N-glycosylation sites occupied by this type of glycans, our aim was to develop a novel high-throughput and cost-effective glycoproteomic workflow for N-glycosylation analysis of human C3 to reveal the possible role of C3 glycosylation in type 1 diabetes development.
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Project description:Systemic lupus erythematosus is a chronic autoimmune disease with multifactorial ethiopathogenesis. The complement system is involved in both the early and late stages of disease development and organ damage. To better understand autoantibody mediated complement consumption the GAPAID consortium examined ex vivo immune complex formation on autoantigen arrays. We recruited patients with SLE (n=211), with other systemic autoimmune diseases (n=65) and non-autoimmune control subjects (n=149) in two rheumatology tertiary care centers. Standard clinical and laboratory data were collected from all subjects and serum complement levels were determined in SLE patients. The genotype of SNP rs1143679 in the ITGAM gene was also determined. On-chip formation of immune complexes was examined using a functional immunoassay on autoantigen microarray. The amount of antigen-bound IgM, IgG and complement C4 and C3 was quantified on autoantigens comprising nucleic acids, proteins and lipids. Our results show that the relatively high complement consumption of nucleic acids is further increased upon binding of IgM and IgG. This is true even when serum complement levels are decreased due to complement consumption in SLE patients. A negative correlation between serum complement levels and ex vivo complement deposition on nucleic acid autoantigens is demonstrated. On the contrary, most protein and lipid autoantigens show positive correlation with C4 and C3 levels. Genetic analysis reveals that the non-synonymous variant rs1143679 in complement receptor type 3 is associated with an increased production of anti-dsDNA IgG antibodies. Notwithstanding, homozygous carriers of the previously reported susceptible allele (AA) have lower levels of dsDNA specific IgM among SLE patients. Regarding organ involvement we find that besides anti-C1q IgG, low levels of dsDNA specific IgM and low complement C4 binding to C1q are also associated with renal injury. In summary, nucleic acids maintain a skewed complement deposition balance when bound by IgG and IgM, depleting the early classical complement pathway from other physiological processes. Dysfunction of the receptor responsible for complement-mediated apoptotic debris removal promotes the development of autoantibodies targeting nucleic acids. These observations provide serological and genetic evidence for complement-mediated clearance deficiency of apoptotic debris in lupus.
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Project description:The most abundant and central component, glycoprotein C3, contributes to the development of type 1 diabetes by enhancing the organ-specific autoimmune inflammatory processes. It is known that changes in glycosylation can modulate inflammatory responses and we recently showed that children at the onset of type 1 diabetes have a higher proportion of oligomannose glycans in plasma N-glycome compared to their healthy siblings. Due to fact that C3 contains two N-glycosylation sites occupied by this type of glycans, our aim was to develop a novel high-throughput and cost-effective glycoproteomic workflow for N-glycosylation analysis of human C3 to reveal the possible role of C3 glycosylation in type 1 diabetes development.
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Project description:Rhabdomyolysis is a severe condition caused by skeletal muscle damage, leading to acute kidney injury (AKI). We demonstrate that complement has a direct pathogenic role in rhabdomyolysis-induced AKI. Deposition of C3d in the tubules of patients and mice correlated with rhabdomyolysis-induced AKI. Moreover, C3-defiient mice with rhabdomyolysis had preserved renal function. Mechanistically, C3-deficiency attenuated strongly inflammatory and apoptotic components of the renal transcriptome, perturbed by rhabdomyolysis. Complement was activated intrarenal by the lectin pathway via collectin-11. It proceeded in a C4-bypass manner and was amplified by heme-activated alternative pathway. Therefore, complement and heme are promising therapeutic targets for rhabdomyolysis-induced AKI.
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