Molecular mimicry between Mycobacterium leprae proteins (50S ribosomal protein L2 and Lysyl-tRNA synthetase) and myelin basic protein: a possible mechanism of nerve damage in leprosy.

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.

journal_name

Microbes Infect

journal_title

Microbes and infection

authors

Singh I,Yadav AR,Mohanty KK,Katoch K,Sharma P,Mishra B,Bisht D,Gupta UD,Sengupta U

doi

10.1016/j.micinf.2014.12.015

subject

Has Abstract

pub_date

2015-04-01 00:00:00

pages

247-57

issue

4

eissn

1286-4579

issn

1769-714X

pii

S1286-4579(14)00337-2

journal_volume

17

pub_type

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