%0 journal article
%@ 1074-7613
%A Neves, P., Lampropoulou, V., Calderon-Gomez, E., Roch, T., Stervbo, U., Shen, P., Kuehl, A.A., Loddenkemper, C., Haury, M., Nedospasov, S.A., Kaufmann, S.H.E., Steinhoff, U., Calado, D.P., Fillatreau, S.

%D 2010
%J Immunity
%N 5
%P 777-790 
%R doi:10.1016/j.immuni.2010.10.016
%T Signaling via the MyD88 Adaptor Protein in B Cells Suppresses Protective Immunity during Salmonella typhimurium Infection
%U https://doi.org/10.1016/j.immuni.2010.10.016
5 
%X The myeloid differentiation primary response gene 88 (Myd88) is critical for protection against pathogens. However, we demonstrate here that MyD88 expression in B cells inhibits resistance of mice to Salmonella typhimurium infection. Selective deficiency of Myd88 in B cells improved control of bacterial replication and prolonged survival of the infected mice. The B cell-mediated suppressive pathway was even more striking after secondary challenge. Upon vaccination, mice lacking Myd88 in B cells became completely resistant against this otherwise lethal infection, whereas control mice were only partially protected. Analysis of immune defenses revealed that MyD88 signaling in B cells suppressed three crucial arms of protective immunity: neutrophils, natural killer cells, and inflammatory T cells. We further show that interleukin-10 is an essential mediator of these inhibitory functions of B cells. Collectively, our data identify a role for MyD88 and B cells in regulation of cellular mechanisms of protective immunity during infection.