Deborah V. Novack

This study shows osteoclasts support S. aureus intracellular growth by providing nutrients and a blunted antimicrobial response.

This study shows that LAIR1 deficiency in mice leads to excessive inflammation during S. aureus infection, similar to CTCL, which increases tissue damage without improving infection control.

This study shows S. aureus inhibits NLRP3 inflammasome activation in macrophages during early infection but not late infection, reducing bacterial load and pyroptosis.

The paper shows Tmem178 suppresses NLRP3 inflammasome activation in osteoclasts by limiting calcium release, preventing excessive bone resorption.

This study shows that the CTCF binding site in HTLV-1 regulates viral pathogenesis by affecting proviral load, Tax expression, and T-cell activation in humanized mice.

This study shows HTLV-1 infected T cells release small extracellular vesicles that promote bone loss by stimulating osteoclasts, independent of RANKL expression.