It is therefore tempting to propose the existence of a possible link between CT-X expression in BC and loss of Xi. These considerations, however, are complicated by our finding that CT-X expression is not limited to the TN BLC group, as a fraction of CT-X expressing HR2 tumors in this study were positive for HER2, whose over- expression identifies a subgroup of BC with molecular character- istics distinct from BLC. The finding that patients with primary BC bearing sometimes relatively small ESO-expressing tumors can mount significant serological responses to ESO is somewhat unexpected, with respect to previous studies that have reported serological responses to ESO in patients bearing significant tumor load, that in some instances become ESO Ab2 after removal of the tumor. These results could imply a particularly high immunogenicity of BC or/and that the primary lesion may not represent the actual total tumor mass present at diagnosis in these patients. Interestingly however, we found that the presence of ESO Ab in patients with ESO-expressing BC correlates with AZ 960 the presence of the tumor in the local lymph nodes, suggesting that the latter may be required for the development of spontaneous anti-tumor response. Another important implication of our findings is that ESO may represent a highly specific marker for the detection of tumor cells outside the primary tumor site, i.e. AZD2281 in the circulation, lymph nodes or bone marrow. In conclusion, the results of our study indicate that the presence of circulating antibodies to ESO identifies a group of HR2 BC with frequent ESO expression and, together with the assessment of antigen expression in the tumor, may be instrumental for the selection of patients who may benefit from recently developed highly immuno- genic ESO-based vaccines. Anti-cancer vaccination as a complement for standard therapy is particularly attractive in this group of patients, including those bearing TN tumors, for whom therapeutic options are limited, and for patients with HER2+ER2 tumors where it may be combined with trastuzumab. Host immune responses are important mechanisms that significantly contribute to the infection process. Different patho- gens use different strategies to either escape or modulate host immune responses. The level and nature of immune responses mainly depends upon the type of infection and the site of involvement. Hence, modulation of immune responses through host or pathogen traits can have a bearing on the outcome of an infection. This phenomenon is especially important in immuno- compromised hosts, for example, in nosocomial settings. P. aeruginosa is a notorious opportunistic pathogen that is difficult to eradicate with conventional antibiotic therapy. Telford et al. carried out the first direct analysis of the effects of OdDHL on myeloid cells involved in the immune response. OdDHL is known to stimulate various host signalling pathways as a mechanism for inhibiting or activating immune cell responses. The immunomodulatory effect that is subsequently generated has led to the hypothesis that QS modulates T-cell responses away from host protective helper T host responses. An increasing body of evidence suggests that OdDHL can interact with different eukaryotic cells, such as epithelial cells and fibroblasts and induce Th2- mediated inflammatory responses as well. In all of the earlier studies, synthetic OdDHL have been employed. Although various studies have reported 98–99% homology between synthetic acyl homoserine lactones and natural AHLs, the biological response to synthetic AHLs may not be the same to that observed with natural AHLs.