@misc{neves_signaling_via_2010, 
author={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.},
title={Signaling via the MyD88 Adaptor Protein in B Cells Suppresses Protective Immunity during Salmonella typhimurium Infection},
year={2010},
howpublished = {journal article},
doi = {https://doi.org/10.1016/j.immuni.2010.10.016},
abstract = {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.},
note = {Online available at: \url{https://doi.org/10.1016/j.immuni.2010.10.016} (DOI). Neves, P.; Lampropoulou, V.; Calderon-Gomez, E.; Roch, T.; Stervbo, U.; Shen, P.; Kuehl, A.; Loddenkemper, C.; Haury, M.; Nedospasov, S.; Kaufmann, S.; Steinhoff, U.; Calado, D.; Fillatreau, S.: Signaling via the MyD88 Adaptor Protein in B Cells Suppresses Protective Immunity during Salmonella typhimurium Infection. Immunity. 2010. vol. 33, no. 5, 777-790. DOI: 10.1016/j.immuni.2010.10.016}}