Submicroscopic infections that are highly prevalent in all malaria endemic settings [31] appeared to provide sufficiently high levels of antigen exposure to maintain

Selleck Crizotinib antibody titres. Our findings confirm observations in Kenyan children where antibody boosting was observed in the absence of patent malaria infections and provide evidence in support of their hypothesis that this could be explained by submicroscopic infections [32]. Our data also offer support for the hypothesis that circulating antimalarial antibodies in children derive mainly from short-lived plasma cells [33] but that long-lived plasma cells may be the major source of antibodies in older individuals [34]. Finally, the very rapid decline – in all age groups – in titres of antibodies to mosquito salivary gland antigens indicates that these antigens fail to induce long-lived plasma cells, suggesting that the antibodies may emanate from ‘innate’ or ‘natural’ B1 cells or that the antigens activate B cells in a T-cell

independent manner (35). We are grateful to the Apac district’s inhabitants for their participation to the study; we also thank CAL 101 Sam Edweo and Dorcus Akello for their contribution during the field work. This study was supported by the FIGHTMAL project, receiving funding from the European Community’s Seventh Framework Programme [FP7/2007-2013] under grant agreement PIAP-GA-2008-218164. “
“In certain infection sites or tumor tissues, the disruption of homeostasis can give rise to a hypoxic microenvironment, which, in turn, can alter

the function of different immune cell types and favor the progression of the disease. Natural killer (NK) cells are directly involved in the elimination of virus-infected or transformed cells, however it is unknown whether their function is affected by hypoxia or not. In this study, we show that NK cells adapt to a hypoxic this website environment by upregulating the hypoxia-inducible factor 1α. However, NK cells lose their ability to upregulate the surface expression of the major activating NK-cell receptors (NKp46, NKp30, NKp44, and NKG2D) in response to IL-2 (or other activating cytokines, including IL-15, IL-12, and IL-21). These altered phenotypic features correlate with reduced responses to triggering signals resulting in impaired capability of killing infected or tumor target cells. Remarkably, hypoxia does not significantly alter the surface density and the triggering function of the Fc-γ receptor CD16, thus allowing NK cells to maintain their capability of killing target cells via antibody-dependent cellular cytotoxicity. This finding offers an important clue for exploitation of NK cell in antibody-based immunotherapy of cancer. As a component of innate immunity, natural killer (NK) cells play an important role in the control of virus infections and in cancer immune surveillance [1-5].