In an effort to explain the control exerted by each of these host factors, an evaluation was made of the corresponding immune response. Since cellular immunity is critical in controlling Brucella infection, splenocytes were used to characterize the role of TLR2, TLR4 and MyD88 in the development of cellmediated adaptive immunity against Brucella. Finding that the loss of TLR2, TLR4 and MyD88 had no demonstrable effect on the development of memory T cell response against Brucella infection was initially a surprise (Figure 4) . However, recent experiments have revealed a disruption of TLR signaling resulting from enhanced degradation of MyD88-adaptor like protein (MAL) that is consistent with previous reports documenting a minimal role for TLR signaling in memory T cell development against other viral and bacterial infections (Way et al., 2003; Fremond et al., 2004; Heer et al., 2007; Seibert et al., 2010; McBride et al., 2011) . These results are also in agreement with a recent study showing that IRAK4 (interleukin-1 receptor associated kinase 4), one of the kinases recruited by MyD88 upon stimulation, is not required for generation of CD4+ and CD8+ T cells producing IFN-γ in the late stage of Brucella infection (Oliveira et al., 2011) . These results suggest that TLR-independent signaling is likely involved in the development of cellular adaptive immunity against Brucella.