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. Author manuscript; available in PMC: 2014 Mar 15.
Published in final edited form as: J Immunol. 2013 Feb 1;190(6):2756–2766. doi: 10.4049/jimmunol.1202697

Figure 10. The role of B1a cells in tularemia.

Figure 10

(A) Resident macrophages produce IL-12 in response to dead and/or lysing SchuS4 following antibiotic therapy. (B) IL-12 provokes NK/NKT cells to produce IFN-γ, which then (C) activates newly infected macrophages to kill SchuS4. However, B1a cells secrete IL-10 in response to dead bacteria (D). This IL-10 down regulates IL-12 production from macrophages, which in turn results in suboptimal IFN-γ responses from NK/NKT cells and poor control of SchuS4 replication among infected macrophages.