In contrast to wild type animals, mice double-deficient for TLR2 and 4 were unable to control the replication of the bacteria and succumbed to progressive pneumonia. Moreover, although many immune responses in vivo, such as the secretion of proinflammatory Perifosine 157716-52-4 cytokines and chemokines, depended almost exclusively on TLR2, the survival of infected mice required the presence of TLR2 but also of TLR4. Unexpectedly, TLR2/4 double-deficient but not TLR2-deficient mice displayed upon infection with the microorganism significantly higher pulmonary levels of IFNc than wild type mice. TLRs also influence the adaptive immune response. Thus, mice lacking MyD88, the most important adapter molecule of the TLRsignaling cascade, failed to mount a TH1 response upon immunization with the model antigen ovalbumin in complete Freund’s adjuvant while antigen-specific TH2 responses were not impaired. In particular, antigen-specific T-cells from MyD88- deficient mice were unable to produce IFNc, but secreted TH2 cytokines like IL-13 and IL-4 at least as efficiently as T-cells from wild type mice. Likewise, it was shown that endotoxin-stimulated wild type dendritic cells induced allogeneic CD4+ T-cells to secrete IFNc while MyD88-deficient allogenic dendritic cells only stimulated a TH2 response. However, upon vaccination of MyD88-deficient mice with Mycobacterium bovis BCG a TH1 response was observed as in wild type mice. Interestingly, the adaptive immune response induced by the vaccination was only partially effective to prevent the lethal outcome of a challenging Mycobacterium tuberculosis infection in MyD88-deficient mice. In summary, the influence of MyD88 on adaptive immune responses appears to depend substantially from the model system used. Here, we explored adaptive immune responses in mice lacking TLR2 and TLR4 upon pulmonary infection with C. pneumoniae. The results demonstrate that an increased IFNc-release by the adaptive immune system in the absence of both TLRs was associated with a lower frequency of regulatory T-cells. However, the cytokine was unable to trigger the release of NO by TLR2/4 double-deficient bone marrow-derived macrophages. The latter finding presumably contributes to the increased lethality observed in TLR2/4 double-deficient mice. The common bed bug, Cimex lectularius was a well established pest in the United States, and other developed nations, at the turn of the 20th century. However, due to the widespread use of DDT, bed bugs were essentially eradicated from U.S. homes and apartments by the 1950s. While DDT was initially effective for bed bug control, resistance to the cyclodienes was well documented among different bed bug populations by 1958. The National Pest Control Association’s initial recommendation for combating DDT-resistant bed bug populations was malathion. Yet, while malathion further reduced the incidence of bed bug infestations in developed nations, bed bugs had developed resistance to organophosphate insecticides, including malathion by the 1960s.