Mi-Jeong Kim

TL;DR: The progression of tuberculosis from a latent, subclinical infection to active disease that culminates in the transmission of infectious bacilli is determined locally at the level of the granuloma, and it is indicated that pathogen-induced dysregulation of host lipid synthesis and sequestration serves a critical role in this transition.

TL;DR: Molecular and biochemical evidence is provided that the development of the human TB granuloma to caseation correlates with pathogen‐mediated dysregulation of host lipid metabolism.

TL;DR: It is demonstrated that the macrophage receptor with collagenous structure (MARCO), a class A scavenger receptor, is utilized preferentially to “tether” TDM to themacrophage and to activate the TLR2 signaling pathway.

TL;DR: Mycobacterium tuberculosis remains one of the most pernicious of human pathogens, and current vaccines are ineffective, and drugs, although efficacious, require prolonged treatment with constant medical oversight.

TL;DR: Investigating if the ER stress pathway is activated during TB infection found that apoptosis was more abundant in granulomas as compared to non-granulomatous tissue isolated from patients with pulmonary TB, and apoptosis correlated with CHOP expression in areas surrounding the centralized areas of caseation.