Moreover, since it is a cellular system, it is possible to do in vitro functionality studies like ADCC and complement activation. This makes the CHO-ldlD MUC1 system complementary to the previously published methods to detect MUC1 serum antibodies, since the clinical significance of underglycosylated MUC1-antibodies in relation to cancer is largely unknown. In conclusion, we report on a cellular, flow cytometry-based technique to detect serum MUC1-Tn antibodies. We show that it is a unique system to detect antibodies binding to the native underglycosylated MUC1 protein and can be effectively

used for antibody monitoring and functional assays. “
“Staphylococcus aureus (S. aureus) causes a diverse arsenal of infections, ranging from superficial skin infections (furuncles and impetigo) to invasive

infections such as abscesses, pneumonia, endocarditis, and AZD4547 solubility dmso bacteraemia ( Lowy, 1998). Little is known about the precise physiological role of many if not most S. aureus antigens that are important in colonization and infection. For some infections, some or at least one of the S. aureus antigens important during infection are known. For example, superantigens such as TSST-1 are predominant in Toxic Shock Syndrome ( Fraser and Proft, 2008); staphylococcal enterotoxins are known to cause food poisoning ( Le Loir et al., 2003); and Panton Valentine Leukocidin is involved in necrotizing pneumonia ( Brown et al., 2009b). Immunogenicity of antigens in these processes can be studied by assessing the antigen-specific antibody responses elicited. It is known that levels of antibodies to toxic shock syndrome toxin 1 (TSST-1), Daporinad purchase staphylococcal enterotoxin A (SEA), and clumping factors A and B (ClfA and ClfB) are significantly higher in persistent carriers of S. aureus than in noncarriers ( Verkaik et al., 2009a). Colonized children have higher IgG levels against chemotaxis inhibitory protein of S. aureus (CHIPS), extracellular

fibrinogen-binding protein (Efb), and iron-responsive surface determinant H (IsdH), and higher IgA levels against CHIPS, iron-responsive surface determinant A (IsdA), and IsdH than non-colonized children in both the first and second years of life ( Verkaik et al., 2009b). Although for instance the course of the humoral immune response in S. aureus bacteraemia patients as well as in pediatric patients infected with community-associated Silibinin S. aureus has been investigated, the importance and therapeutic effect of antibody induction in many other diseases remain enigmatic ( Brown et al., 2009a and Verkaik et al., 2010a). While clinical studies remain the most informative in this respect, animal models of S. aureus infection enable investigation of antibody responses to specific S. aureus antigens under similar conditions of S. aureus colonization and infection as are encountered by humans. In this way animal studies may provide insight into the potential role of S.