@article{27128, keywords = {Reactions, leprosy, Bangladesh}, author = {Bahia El Idrissi N and Hakobyan S and Ramaglia V and Geluk A and Morgan P and Das PK and Baas F}, title = {Complement Activation In Leprosy: A Retrospective Study Shows Elevated Circulating Terminal Complement Complex In Reactional Leprosy.}, abstract = {
Mycobacterium leprae (M. leprae) infection gives rise to the immunologically and histopathologically classified spectrum of leprosy. At present several tools for the stratification of patients are based on acquired immunity markers. However, the role of innate immunity, particularly the complement system, is largely unexplored. The present retrospective study was undertaken to explore whether the systemic levels of complement activation components and regulators can stratify leprosy patients, particularly in reference to the reactional state of the disease. Serum samples from two cohorts were analyzed. The cohort from Bangladesh included multibacillary (MB) patients with (n=12) or without (n=46) reaction (R) at intake and endemic controls (n=20). The cohort from Ethiopia included paucibacillary (PB; n= 7) and MB (n= 23) patients without reaction and MB (n=15) patients with reaction. The results showed that the activation products terminal complement complex (TCC) (p ≤0.01), C4d (p ≤0.05) and iC3b (p ≤0.05) were specifically elevated in Bangladeshi patients with reaction at intake compared to endemic controls. In addition, levels of the regulator Clusterin (p ≤0.001 without R; p<0.05 with R) were also elevated in MB patients irrespective of a reaction. Similar analysis of the Ethiopian cohort confirmed that irrespective of a reaction, serum TCC levels were significantly increased in patients with reactions compared to patients without reactions (p ≤0.05). Our findings suggests that serum TCC levels may prove to be a valuable tool in diagnosing patients at risk of developing reactions. This article is protected by copyright. All rights reserved.
}, year = {2016}, journal = {Clinical and experimental immunology}, issn = {1365-2249}, url = {https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4872382/pdf/CEI-184-338.pdf}, doi = {10.1111/cei.12767}, language = {eng}, }