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|dc.description.abstract||Mycobacterium tuberculosis (Mtb) is able to replicate and survive in macrophage and suppress host immune response. But detailed mechanism that Mtb facilitates to enhance intracellular survival is unclear. Here, we found that Cluster of Differentiation 82 (CD82) plays critical role in Mtb intracellular survival and inflammation, and epigenetic modification participated in host anti-bacterial responses. CD82 expression is up-regulated significantly by Mtb virulent strain H37Rv, but slightly by Mtb avirulent strain H37Ra. In CD82-overexpression manner, various mycobacterial survival increased. In contrast, CD82 deficient condition, intracellular survival of mycobacteria decreased and antibacterial response enhances against Mtb infection. DNA methylation level in CD82 promoter region is changed by Mtb H37Rv infection. Mtb H37Ra infection increases DNA methyltransferases mRNA level. In addition, we show that DNA methylation inhibitor, 5-Aza-2’- deoxycytidine, treatment is concerned in increasing CD82 level. These data indicate that Mtb H37Rv is able to survive against host immune response by regulating DNA methylation of CD82 promoter region. Thus, the studies in roles of CD82 will provides opportunities for finding therapeutic candidates about tuberculosis.||-|
|dc.title||The Role of CD82 in Mycobacterium tuberculosis Infection||-|
|dc.title.alternative||결핵균 감염에 대한 CD82 역할 연구||-|
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