from single photon producing nitrogenvacancy (NV) color centers consisting of a substitutional nitrogen atom next to a vacancy that is engineered artificially in the diamond lattice. The nanoscale effects related to artificially engineered NV color centers attracted important attention to diamond due to applications ranging from quantum computing to cell imaging. [2][3][4] The luminescence from NV centers is extremely stable without any photobleaching or photoblinking [5][6][7] and compared to better known quantum dots, ND brings additional advantages such as high biocompatibility [8,9] and simple C-surface chemistry. [10,11] This allows grafting of biomolecules that are interesting for cellular targeting [12,13] or biomolecular drug delivery. [14][15][16] However, for very small ND particles (5 nm) blinking of NV centers was observed, [17] showing that the surface effects are of importance for stabilization of NV luminescence properties.Here we describe how the surface chemistry effects can make the ND bulk luminescence sensitive to chemical processes ongoing at the ND surface, with the aim of using ND for monitoring a chemical environment such as surface charges or pH, cellular DNA/RNA hybridization, interaction with cell receptors, etc. The proposed method is based on the control of an electronic chemical potential at the

A diversity of high-affinity oligosaccharide ligands are identified for NKR-P1, a membrane protein on natural killer (NK) cells which contains an extracellular Ca(2+)-dependent lectin domain. Interactions of such oligosaccharides on the target cell surface with NKR-P1 on the killer cell surface are crucial both for target cell recognition and for delivery of stimulatory or inhibitory signals linked to the NK cytolytic machinery. NK-resistant tumour cells are rendered susceptible by preincubation with liposomes expressing NKR-P1 ligands, suggesting that purging of tumour or virally infected cells in vivo may be a therapeutic possibility.

Intestinal microbiota are considered to play an important role both in colorectal tumor development and in the modulation of mucosal immunity. Studies on animals reared in germ-free (GF, without intestinal microbiota) versus conventional (CV, with regular microbiota colonization of the bowel) conditions can aid in clarifying the influence of bacteria on carcinogenesis and the anticancer immune response. The capability of the intestinal environment to modulate anticancer immunity not only at the mucosal but also at the systemic level is still an open question. In our study we found that, following the same protocol of colorectal cancer induction, GF rats developed less and smaller tumors than CV rats. The GF rats that did not develop cancer also presented a better anticancer immune response with an increase in NK, NKT, CTL, B cells and cytotoxicity in peripheral blood. We hypothesize that the lower antigenic challenge and the absence of the 'physiological inflammation', caused by the commensal microbiota in the gut of CV rats, may enhance the capability of the GF rats to develop more efficacious anticancer immune responses. The different levels of tolerance/ regulatory mechanisms in GF versus the CV animals may modulate the anticancer response not only at the mucosal but also at the systemic immunity level.