C5aR contributes to the weak Th1 profile induced by an outbreak strain of Mycobacterium tuberculosis

Performance of a highly successful outbreak strain of Mycobacterium tuberculosis in a multifaceted approach to bacterial fitness assessment

“…This was the case for the non-prosperous 410 strain, a variant of the M strain, contemporary to the outbreak, which caused a single case in two decades despite having numerous opportunities to be transmitted (Yokobori et al, 2013). We have previously shown that the M strain can manipulate macrophage cell death (Yokobori et al, 2012), innate (Yokobori et al, 2013;Yokobori et al, 2012) and adaptive immune responses (Basile et al, 2011;Geffner et al, 2009;Sabio et al, 2017), as well as T cell-mediated cytotoxicity (Geffner et al, 2014), suggesting that it efficiently evades host immunity. However, we still have no direct evidence, other than epidemiology, that can account for the enhanced fitness of the M strain, as its axenic and intracellular growth was slower compared to the laboratory strain H37Rv and 410 (Yokobori et al, 2013).…”

The Controversial C5a Receptor C5aR2: Its Role in Health and Disease

“…Neutrophils from patients with familial Mediterranean fever had lower C5aR2 mRNA expression [40]. The CD14 + -circulating monocytes from tuberculosis patients expressed higher surface levels of C5aR2, compared to those from healthy donors [41]. But it was C5aR1, not C5aR2 who participated in the inhibition of Th1 polarization induced by highly pathogenic Mycobacterium tuberculosis M. strain.…”