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Altered Expression of Complement Regulatory Proteins CD35, CD46, CD55, and CD59 on Leukocyte Subsets in Individuals
Nitesh Mishra1, Madhav Mohata1, Rajeev Narang2
1Department of Biochemistry, All India Institute of Medical Sciences, New Delhi, India.
Insights
Coronary artery disease (CAD) patients show altered levels of complement regulatory proteins (Cregs). Lower Cregs and higher complement activation markers were found in CAD, with specific changes on immune cells potentially indicating disease severity.
Area of Science:
- Immunology
- Cardiovascular Medicine
Background:
- Membrane complement regulatory proteins (Cregs) are implicated in coronary artery disease (CAD) pathophysiology based on animal studies.
- Understanding Cregs' role in human CAD is crucial for developing targeted therapies.
Purpose of the Study:
- To investigate plasma levels and cellular expression of Cregs (CD35, CD46, CD55, CD59) in patients with stable CAD compared to healthy controls.
- To correlate Cregs' expression with disease severity and complement activation markers.
Main Methods:
- Recruited 100 CAD patients and 100 healthy controls.
- Quantified plasma Cregs, soluble Cregs, complement activation marker C3c, MASP-2, PAF-AH, and cytokines using ELISA.
- Assessed Cregs surface expression on leukocytes (granulocytes, lymphocytes, monocytes) via flow cytometry.
- Determined Cregs mRNA expression in total leukocytes using quantitative PCR.
Main Results:
- CAD patients exhibited high plasma C3c levels, indicating complement activation, and significantly lower overall Cregs.
- Reduced surface expression of CD46 and CD55 on lymphocytes, monocytes, and granulocytes was observed in CAD patients.
- Elevated surface expression of CD35 and CD59 on granulocytes was noted in CAD patients compared to controls.
- High CD59 expression on granulocytes correlated positively with CAD severity.
Conclusions:
- Patients with CAD display dysregulated complement regulatory proteins and heightened complement activation.
- Specific alterations in Cregs expression on immune cells may serve as biomarkers for CAD progression.
- Targeting complement pathways could offer therapeutic strategies for CAD management.
Abstract:
Studies conducted in animal models have suggested that membrane complement regulatory proteins play an important role in the pathophysiology of coronary artery disease (CAD). In this study, a total of 100 individuals, with stable CAD and 100 healthy controls, both groups predominantly male, were recruited. We evaluated the plasma levels of complement regulatory proteins (Cregs) CD35, CD46, CD55, and CD59 and their surface expression on granulocytes, lymphocytes, and monocytes by flow cytometry. The mRNA expression of these Cregs in total leukocytes was determined by quantitative PCR. The soluble forms of Cregs, C3c, Mannose binding protein-associated serine protease 2 (MASP-2), Platelet activating factor-acetyl hydrolase (PAF-AH), and inflammatory cytokines were quantified by ELISA. High plasma levels of C3c, indicative of complement activation, in addition to significantly low levels of Cregs, were observed in CAD patients. A significantly lower expression of CD46 and CD55 on the surface of lymphocytes, monocytes, and granulocytes and higher surface expression of CD35 and CD59 on granulocytes (p < 0.0001) was seen in CAD patients as compared to healthy donors. The high expression of CD59 on granulocytes positively correlated with the severity of disease and may serve as a potential marker of disease progression in CAD.
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