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Abstract
A study was conducted to evaluate role of complement proteins and complementreceptor 1 (CR1) in pathogenesis of Systemic lupus erythematosus (SLE) and Immunecomplex (IC) mediated glomerulonephritis. C3, C4, C3d and CH100 in serum, CR1 inrenal biopsies and RBC showed these parameters to be of great diagnostic andprognostic values in Immune complex mediated diseases. Our study revealed an overalldecrease in levels of CR1, C3, C4 in IC mediated as compared to non - IC mediateddisease. Whereas C3d in case of SLE 247 ± 39 AU/L including IC mediatedGlomerulonephritis (ICGN) 208 ± 51 AU/L was found to be significantly increased(P < 0.05) than normal control 46 ± 6 AU/L. There was no appreciable increase incase of non - 1C mediated GN (61 ± 12 AU/L) CRI among SLE patients (261 ± 141/E)and IC mediated group (270 ± 107/E) was found to be significantly lower (P < 0.05)than normal control (627 ± 132/E) and non - IC GN (550 ± 86/E). C4 values amongSLE, patients were found to be 191 ± 104 mg/L as compared to control (286 ±110 mg/L). The kidney biopsy of type III and type IV lupus nephritis revealed a completeabsence of CR1 in contrast to minimal change diseases. Thus this study revealed thatabove parameters could be a valuable tool for distinguishing IC versus non-IC mediatedkidney diseases.Key Words: Complement receptor 1 (CR1) Glomerulonephritis, SLE.
Highlights
Complement system comprises of multimolecular self assembly of 30 plasma proteins implicated as principal mediators of inflammation, promoting opsonisation and may damage host tissue when there is persistent activation of complement by antigen-antibody complex and deposited in tissues
Fifty-one subjects included in the study consisted of normal controls (n=14) and patients suffering from diseases such as systemic lupus erythematosus (SLE) (n=7) immune complex (IC) mediated (n=10) and non-IC mediated glomerulonephritis (n=20)
Quantitation of complement receptor 1 (CR1) receptors on erythrocytes were measured with patients using ELISA (Anthos Instrument, Austria), coating the wells with patients RBC and mouse monoclonal antibodies to human CR1 receptor
Summary
Complement system comprises of multimolecular self assembly of 30 plasma proteins implicated as principal mediators of inflammation, promoting opsonisation and may damage host tissue when there is persistent activation of complement by antigen-antibody complex and deposited in tissues. The receptor for cleavage fragment of third component of human complement C3b receptor (CR1) is expressed abundantly in erythrocytes, polymorph, monocyte, T and B cells, glomerular podocytes and soluble form in plasma. It plays major role in the disposal of immune complexes from circulation. It serves as regulatory protein by preventing classical and alternative pathway of complement.[1,2]. The deficiency of complement proteins impair the RBC immune complex processing and clearing mechanism and predisposes individuals to immune complex/ auto immune diseases. Estimate the serum complement levels which includes C3, C4, C3d, CH100 and its correlation with CR1 and disease activity
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