Suppressor of cytokine signaling-1 influences bacterial clearance and pathology during the infection with Mycobacterium tuberculosis

ABSTRACT: Tuberculosis results from an interaction between a chronically persistent pathogen counteracted by IFN-g-mediated immune responses. Modulation of IFN-g signaling could therefore constitute a major immune evasion mechanism for M. tuberculosis. SOCS1 plays a major role in the inhibition of IFN-g-mediated responses. We found that M. tuberculosis infection stimulates SOCS1 expression in mouse and human myeloid cells. Significantly higher levels of SOCS1 were induced after in vitro or in vivo infection with virulent M. tuberculosis-than with attenuated M. bovis BCG. Different innate and adaptive immune mechanisms participated in infection-induced SOCS1 expression. SOCS1 hampered M. tuberculosis clearance both in macrophages and during murine infection in vivo. On the other hand, SOCS1 protected

ORGANISM(S): Mus musculus

SUBMITTER: Sabin Bhuju 

PROVIDER: E-GEOD-23508 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress