Both innate and adaptive immunity have been described as contributing to the control of Brucella infection (Baldwin and Parent, 2002; Dornand et al., 2002; Baldwin and Goenka, 2006) . The role of innate immunity against infection by this pathogen has drawn recent attention as a result of awareness of the role of innate immunity in the establishment of infection and the development of adaptive immunity (Weiss et al., 2005; Oliveira et al., 2011) . In contrast, adaptive immunity, including cell-mediated and humoral responses, has been the prominent focus of Brucella research over the past few decades. The innate immune system is composed of a variety of cellular and humoral components, which are the first line of the host defense against invading pathogens. Recognition relies on pattern recognition receptors (PRRs) expressed on/in the cellular components of the innate immune system. Toll-like receptors (TLRs) are the best characterized PRRs. Receptorligand interaction via TLRs induces the production of antimicrobial peptides and proinflammatory cytokines through NF-κB, mitogen-activated protein kinase (MAPK) and other signaling pathways (Kawai and Akira, 2006) . As a result, TLR signaling is critical to development of the host innate immune response, including recruitment of dendritic cells (DCs) and T effector cells, and upregulation of MHC I and II on antigen presenting cells (APCs) and by extension adaptive immunity against infection. 10 TLRs in human and 13 in the mouse have been identified to date (Kawai and Akira, 2006) . TLR2, TLR4, TLR5, and TLR9 recognizing lipopeptide, lipopolysaccharides, flagellin and CpG DNA, respectively, are known to be important in controlling bacterial infections. With the exception of TLR3, the TLRs require the adapter molecule myeloid differentiation factor 88 (MyD88) for signal transduction (Kawai and Akira, 2007) . As expected, MyD88 have been shown to be essential for clearance of Brucella infection from mice (Weiss et al., 2005; Copin et al., 2007; Macedo et al., 2008) .