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Suppressor of cytokine signalling 3 (SOCS3) negatively regulates STAT3 activation in response to several cytokines such as those in the gp130-containing IL-6 receptor family. Thus, SOCS3 may play a major role in immune responses to pathogens. In the present study, the role of SOCS3 in  M. tuberculosis  infection was examined. All  Socs3 fl/fl  LysM cre, Socs3 fl/fl  lck cre  (with SOCS3-deficient myeloid and lymphoid cells, respectively) and  gp130 F/F  mice , with a mutation in gp130 that impedes binding to SOCS3, showed increased susceptibility to infection with  M. tuberculosis . SOCS3 binding to gp130 in myeloid cells conveyed resistance to  M. tuberculosis  infection via the regulation of IL-6/STAT3 signalling. SOCS3 was redundant for mycobacterial control by macrophages  in vitro . Instead, SOCS3 expression in infected macrophages and DCs prevented the IL-6-mediated inhibition of TNF and IL-12 secretion and contributed to a timely CD4+ cell-dependent IFN-γ expression  in vivo . In T cells, SOCS3 expression was essential for a gp130-independent control of infection with  M. tuberculosis , but was neither required for the control of infection with attenuated  M. bovis  BCG nor for  M. tuberculosis  in BCG-vaccinated mice.  Socs3 fl/fl  lck cre  mice showed an increased frequency of γδ+ T cells in different organs and an enhanced secretion of IL-17 by γδ+ T cells in response to infection.  Socs3 fl/fl  lck cre  γδ+ T cells impaired the control of infection with  M. tuberculosis . Thus, SOCS3 expression in either lymphoid or myeloid cells is essential for resistance against  M. tuberculosis  via discrete mechanisms.

Critical and Independent Role for SOCS3 in Either Myeloid or T Cells in Resistance to Mycobacterium tuberculosis