Functional characterization of the complement receptor type 1 and its circulating ligands in patients with
Arsen Arakelyan1, Roksana Zakharyan, Aren Khoyetsyan
1Institute of Molecular Biology, National Academy of Sciences of the Republic of Armenia, 7 Hasratyan St,, 0014, Yerevan, Armenia. aboyajyan@sci.am.
Insights
Schizophrenia is linked to higher levels of C1q-complement-containing immune complexes (C1q-CIC) and increased complement receptor type 1 (CR1) expression on blood cells, particularly erythrocytes. These findings suggest a role for CR1 and C1q-CIC in schizophrenia pathogenesis.
Area of Science:
- Immunology
- Neuroscience
- Genetics
Background:
- Complement system alterations are implicated in schizophrenia.
- Complement receptors and regulators remain understudied in schizophrenia.
- Complement receptor type 1 (CR1) plays a role in immune regulation.
Purpose of the Study:
- Investigate CR1 expression on blood cells in schizophrenia patients.
- Quantify circulating immune complexes (CIC) involving CR1 ligands (C1q, C3d).
- Analyze the functional CR1 C5507G polymorphism in relation to schizophrenia.
Main Methods:
- Compared CR1 expression on erythrocytes, lymphocytes, and monocytes between schizophrenia patients and controls.
- Measured levels of C1q-CIC and C3d-CIC.
- Genotyped the CR1 C5507G polymorphism.
Main Results:
- Schizophrenia patients exhibited increased C1q-CIC levels and elevated CR1 expression on blood cells.
- A higher number of CR1-positive erythrocytes and fewer CR1-positive lymphocytes/monocytes were observed in patients.
- No significant difference in C3d-CIC levels was found between groups.
- The CC genotype of CR1 C5507G was associated with higher CR1 expression on erythrocytes.
Conclusions:
- Schizophrenia is associated with increased CR1 expression and elevated C1q-CIC levels.
- These findings highlight a potential role for CR1 and C1q-CIC in schizophrenia.
- Further research in diverse ethnic groups is recommended for validation.
Background:
Whereas the complement system alterations contribute to schizophrenia, complement receptors and regulators are little studied. We investigated complement receptor type 1 (CR1) expression on blood cells, the levels of circulating immune complexes (CIC) containing ligands of CR1, C1q complement protein and fragments of C3 complement protein (C1q-CIC, C3d-CIC), and CR1 C5507G functional polymorphism in schizophrenia patients and controls.
Results:
We found an increased C1q-CIC level and CR1 expression on blood cells, elevated number of CR1 positive erythrocytes and reduced number of CR1 positive lymphocytes and monocytes in patients compared to controls. No difference in the levels of C3d-CIC between groups was observed. Higher CR1 expression on erythrocytes in CC genotype versus CG+GG for both groups was detected, whereas no difference was observed for other cell populations. Our results indicated that schizophrenia is associated with the increased CR1 expression and C1q-CIC level.
Conclusions:
Our study for the first time indicated that schizophrenia is associated with the increased CR1 expression and C1q-CIC level. Further studies in other ethnic groups are needed to replicate these findings.
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