CD82 hypomethylation is essential for tuberculosis pathogenesis via regulation of RUNX1-Rab5/22

Abstract

Tuberculosis: Evading host defences The tuberculosis-causing bacterium Mycobacterium tuberculosis regulates a tumor suppressor gene in order to survive and grow in host immune cells. Chul-Su Yang and colleagues at Hanyang University, South Korea, have found that the bacterium can stimulate the expression of CD82 in macrophages by removing methyl groups from its DNA sequence. CD82’s hypomethylated region interacts with and activates proteins that interfere with the cell’s ability to mount an inflammatory response and degrade bacteria in specialized intracellular vesicles called lysosomes. The increased survival rate of CD82-deficient mice following infection with tuberculosis and the elevated levels of CD82 protein found in the inflammatory lesions of patients with tuberculosis further support a previously unrecognized role for this protein in M. tuberculosis infection. Targeting CD82-mediated signaling could be a promising approach for designing new therapeutics.