Abstract |
Autoantibodies against various components of host are known to occur in leprosy. Nerve damage is the primary cause of disability associated with leprosy. The aim of this study was to detect the level of autoantibodies and lympho-proliferative response against myelin basic protein (MBP) in leprosy patients (LPs) and their correlation with clinical phenotypes of LPs. Further, probable role of molecular mimicry in nerve damage of LPs was investigated. We observed significantly high level of anti-MBP antibodies in LPs across the spectrum and a positive significant correlation between the level of anti-MBP antibodies and the number of nerves involved in LPs. We report here that 4 B cell epitopes of myelin A1 and Mycobacterium leprae proteins, 50S ribosomal L2 and lysyl tRNA synthetase are cross-reactive. Further, M. leprae sonicated antigen hyperimmunization was responsible for induction of autoantibody response in mice which could be adoptively transferred to naive mice. For the first time our findings suggest the role of molecular mimicry in nerve damage in leprosy.
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Authors | Itu Singh, Asha Ram Yadav, Keshar Kunja Mohanty, Kiran Katoch, Prashant Sharma, Bishal Mishra, Deepa Bisht, U D Gupta, Utpal Sengupta |
Journal | Microbes and infection
(Microbes Infect)
Vol. 17
Issue 4
Pg. 247-57
(Apr 2015)
ISSN: 1769-714X [Electronic] France |
PMID | 25576930
(Publication Type: Journal Article, Research Support, Non-U.S. Gov't)
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Copyright | Copyright © 2015 Institut Pasteur. Published by Elsevier Masson SAS. All rights reserved. |
Chemical References |
- Myelin Basic Protein
- Ribosomal Proteins
- ribosomal protein L2
- Lysine-tRNA Ligase
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Topics |
- Animals
- Demyelinating Diseases
(complications, etiology, microbiology)
- Humans
- Leprosy
(complications, etiology, microbiology)
- Lysine-tRNA Ligase
(physiology)
- Mice
- Mice, Inbred BALB C
(blood)
- Molecular Mimicry
(physiology)
- Mycobacterium leprae
(pathogenicity)
- Myelin Basic Protein
(physiology)
- Rabbits
- Ribosomal Proteins
(physiology)
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