“…Once brucellae achieve intracellular infection, their elimination proves to be more difficult as these have a number of tools to evade the host immune system. As such, brucellae exist in Brucella -containing vacuoles (BCVs; Gomes et al, 2012 ; Celli et al, 2019 ; Roop et al, 2021 ), which traffic in the endocytic pathway incorporating endosomal membrane proteins, e.g., calreticulin and calnexin1, avoiding phagolysosome maturation and killing ( Pizarro-Cerdá et al, 1998 ; Celli et al, 2003 ; Starr et al, 2008 ; Gomes et al, 2012 ; Celli et al, 2019 ; Bhagyaraj et al, 2021 ; Roop et al, 2021 ) in a VirB-dependent fashion ( Celli et al, 2003 ; Starr et al, 2008 ; Gomes et al, 2012 ; Roop et al, 2021 ). To avoid TLR4 and other LPS-sensitive innate detection sensors, Brucella expresses a low endotoxic LPS ( Forestier et al, 2000 ; Martirosyan et al, 2011 ; Conde-Álvarez et al, 2012 ; Byndloss and Tsolis, 2016 ).…”