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Autoimmune Diseases
Volume 2010 (2010), Article ID 470695, 6 pages
Research Article

Fc 𝛾 RIIA Genotypes and Its Association with Anti-C1q Autoantibodies in Lupus Nephritis (LN) Patients from Western India

National Institute of Immunohaematology, Indian Council of Medical Research, 13th floor, KEM Hospital, Parel, Mumbai 400 012, India

Received 10 July 2009; Revised 15 October 2009; Accepted 6 December 2009

Academic Editor: Edmond J. Yunis

Copyright © 2010 Vandana Pradhan et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


To identify Fc 𝛾 RIIA genotypes in Systemic Lupus Erythematosus (SLE) patients and their association with anti-C1q antibodies. Methods. Fc 𝛾 RIIA genotyping was done in eighty Indian SLE patients and eighty healthy controls using allele-specific PCR. Anti-C1q antibodies were measured by ELISA. Results. LN patients showed higher SLEDAI (6–32) as compared to SLE patients without renal manifestations and had SLEDAI between 6–23. Fc 𝛾 RIIA polymorphic frequency in SLE patients was R131/H131 (67.5%), R131/R131 (20%) and H131/ H131 (12.5%) as against that of normal population (62.5%, 10%, and 27.5%), respectively. Sixty two patients (77.5%) showed positivity for anti-C1q antibodies. LN patients showed elevated levels of anti-C1q antibodies ( 2 5 8 . 2 u / m l ± 3 8 . 5 U / m L ) as compared to SLE patients without nephritis ( 1 3 4 . 6 ± 2 4 . 6  U/mL). Among anti-C1q positive patients, 71% had R131/H131 genotype, 22.6% had R131/R131 and remaining 6.4%, patients had H131/H131 genotype. All anti-C1q positive patients with R131/R131 genotype had elevated levels of anti-C1q antibodies (>100 U/ml), whereas among anti-C1q negative patients, none had R131/R131 genotype. Conclusion. This first report on Indian SLE patients supports the hypothesis that Fc 𝛾 RIIA R131 variant over expression may constitute a susceptibility factor for development of severe SLE manifestations in LN patients.