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CCR2-64I and CCR5Δ32 Polymorphisms in Korean Patients with Myasthenia Gravis
Author(s) -
Hyun Sook Kim,
DaeSeong Kim,
Eun Young Lee,
IlNam Sunwoo,
YoungChul Choi
Publication year - 2007
Publication title -
journal of clinical neurology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.208
H-Index - 45
eISSN - 2005-5013
pISSN - 1738-6586
DOI - 10.3988/jcn.2007.3.3.133
Subject(s) - myasthenia gravis , genotype , ccr2 , ccr4 , immunology , chemokine receptor , chemokine , restriction fragment length polymorphism , immune system , allotype , medicine , biology , antibody , gene , genetics
Chemokines participate in the regulation of immune and inflammatory responses by interacting with their receptors, which are primarily expressed on immune and inflammatory cells such as B- and T-lymphocytes and antigen-presenting cells. Chemokines and their receptors are therefore considered to mediate inflammation and tissue damage in autoimmune disorders. Chemokine receptor (CCR) genotypes were recently identified, and the importance of their genetic polymorphisms in some autoimmune and infectious disorders has been demonstrated. To define the roles of the polymorphism of the CCR2 gene at codon 64 (CCR2-64I) and the 32-bp deletion in the coding region of CCR5 (CCR5Delta32) in Korean patients with myasthenia gravis (MG), we compared these genotypes in MG cases and healthy controls and investigated the clinical features associated with these genotypes.

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