JOURNAL ARTICLE
RESEARCH SUPPORT, NON-U.S. GOV'T
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A study on anti-mannose binding lectin (anti-MBL) antibodies and serum MBL levels in Indian systemic lupus erythematosus patients.

Systemic lupus erythematosus (SLE) is a prototype autoimmune disease characterized by systemic inflammation and autoantibody production. Anti-mannose binding lectin (anti-MBL) autoantibodies have been studied in SLE for their possible effect on mannose binding lectin (MBL) levels and functional activity. This study aimed at the detection of anti-MBL autoantibodies in Indian SLE patients and evaluates their relationship with related immunological parameters. Two hundred diagnosed SLE patients from Western India were included in the study where 87 patients were lupus nephritis (LN) (43.5 %) and remaining (56.5 %) were non-LN. Disease activity was assessed using the Systemic Lupus Erythematosus Disease Activity Index (SLEDAI). Anti-MBL autoantibodies to IgG and IgM isotypes, anti-C1q autoantibodies, MBL levels and circulating immune complex levels were detected by ELISA. C3, C4 and CRP levels were detected by nephelometer. Anti-MBL autoantibodies were detected in 52 % SLE patients, where 55 % had IgG-anti-MBL, 33.8 % had IgM-anti-MBL and 11.3 % had both subclasses. Low MBL levels were present in 64.4 % anti-MBL positives as compared to 61.5 % in anti-MBL negatives. Among anti-MBL positives, 74 % had anti-C1q antibodies, whereas 41.7 % of anti-MBL negatives had anti-C1q autoantibodies (p = 3.45E06). An inverse correlation was observed between serum MBL and CIC levels. A statistically significant difference was noted between anti-MBL positives and anti-MBL negative patients with hsCRP levels (p = 0.002). Occurrence of infections was higher among anti-MBL positives (65 %) as compared to anti-MBL negatives (35 %). The difference between SLEDAI scores among anti-MBL-positive and anti-MBL-negative groups was statistically insignificant. Anti-MBL autoantibodies in SLE patients can influence functional activity of MBL and have a significant role in SLE disease pathogenesis.

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