Disease severity and mortality can be independently regulated in a mouse model of experimental graft versus host disease.

Graft versus host disease (GVHD) is the major limitation of allogeneic hematopoietic stem cell transplantation (HSCT) presenting high mortality and morbidity rates. However, the exact cause of death is not completely understood and does not correlate with specific clinical and histological parameters of disease. Here we show, by using a semi-allogeneic mouse model of GVHD, that mortality and morbidity can be experimentally separated.

Neuroimmunoendocrine regulation of the prion protein in neutrophils.

The prion protein (PrP(C)) is a cell surface protein expressed mainly in the nervous system. In addition to the role of its abnormal conformer in transmissible spongiform encephalopathies, normal PrP(C) may be implicated in other degenerative conditions often associated with inflammation. PrP(C) is also present in cells of hematopoietic origin, including T cells, dendritic cells, and macrophages, and it has been shown to modulate their functions.

[The knowledge of the population of Viçosa, MG, about the ways of AIDS transmission].

AIDS is a major public health problem reaching all social strata. Knowing about the ways of transmission is a way of preventing the disease. For evaluating the level of knowledge of the population of the city of Viçosa about AIDS transmission, a questionnaire about the ways of transmission of the disease based on studies made in Europe was applied to 376 individuals.

G-CSF-treated granulocytes inhibit acute graft-versus-host disease.

It has been shown that in vivo and in vitro treatment with G-CSF induces the generation of low-density granulocytes (LDGs), which copurify with PBMCs and inhibit IFN-gamma production by human T cells. These results prompted us to postulate an immunomodulatory role for LDGs in acute graft-versus-host disease (aGVHD). Here it is shown that in the mouse experimental model, in vivo and in vitro G-CSF treatment generates LDGs capable of inhibiting 80% of T-cell IFN-gamma production.