All data are represented as n unless otherwise noted

may be 25036716 used in tumor treatment sparing in 20020776 NK cells the activating receptor-mediated release of antitumor soluble factors as FasL and TNFa and ADCC activity. incubated for 36 h or cultured for 6d with the indicated drugs or solvent. Then, cytolysis of P815 cells was triggered with mAbs to the indicated receptors and analyzed in a 4 h 51Cr release assay at the E:T ratio of 10:1 or 1:1. UnmAb: unrelated mAb matched for isotype as negative control. Basal: cytolysis detected in the absence of any mAb. Results are expressed as percentage of 51Cr specific release and are the mean6SD of six experiments. Effect of RS1 biological activity fluvastatin on NK cell surface markers expression. NK cells isolated from peripheral blood were cultured in medium alone or supplemented with IL2 , with solvent of fluvastatin or fluvastatin for 3d.. Forward and side scatter analysis of NK cells, R1: gate on living cells.. Surface expression of the indicated molecules on R1 gated NK cells evaluated by indirect immunofluorescence using the specific mAbs followed by PE-GAM. NK cells stained with an unrelated mAb as negative control are indicated by the black thin line histogram. Samples were run on a CyAnADP flow cytometer and results are expressed as Log red fluorescence intensity vs number of cells. In each subpanel MFI of cells stained with the corresponding mAb is indicated.. NK cells cultured with IL2 in medium alone or as in panel C were analyzed on day 6 for the indicated activating or inhibiting cell surface receptors with specific mAbs. Samples were run on a CyAnADP flow cytometer. Results are expressed as mean Log red fluorescence intensity and are the mean6SD from 6 independent experiments. Statistical significance p,0.0001 p,0.001 versus control. ns: not significant. ~~ Malaria is among the deadliest infectious diseases, killing in excess of one million people every year, mostly of African children under the age of five. Transmission is entirely dependent on the completion of the life cycle of Plasmodium, the causative agent of malaria, in its mosquito vector. After ingestion of an infectious blood meal, Plasmodium gametocytes differentiate into male and female gametes that fertilize to generate a diploid zygote. After a round of DNA replication, the tetraploid zygote differentiates into a motile ookinete. At approximately 24 h after ingestion the ookinete invades the mosquito midgut and differentiates into sessile oocysts. Within 7 to 14 days, thousands of sporozoites are released from each oocyst into the mosquito hemocoel. Sporozoites must successfully invade the salivary glands to ensure transmission when the infected mosquito bites and inoculates sporozoites into a new individual. The parasite life cycle in its mosquito host is complex, and dramatic losses in parasite numbers occur at each stage of Plasmodium development. Ookinete midgut invasion represents the largest bottleneck in parasite numbers, as ookinetes must overcome the effects of the mosquito midgut microbiota and the innate immune responses in order to successfully transition into an oocyst. The mosquito midgut microbiota is very dynamic, with dramatic fluctuations based upon life-stage, nutritional status, and age. After a blood meal, mosquito commensal bacteria undergo changes in their population structure to enrich for enteric gram-negative bacteria capable of surviving the harsh, digestive environment of the mosquito midgut. Within this nutrient-rich environment, bacteria reach high numbers at a time th