Rapamycin Improves the Response of Effector and Memory CD8 T Cells Induced by Immunization With ASP2 of .

Deficiency in memory formation and increased immunosenescence are pivotal features of infection proposed to play a role in parasite persistence and disease development. The vaccination protocol that consists in a prime with plasmid DNA followed by the boost with a deficient recombinant human adenovirus type 5, both carrying the ASP2 gene of , is a powerful strategy to elicit effector memory CD8 T-cells against this parasite. In virus infections, the inhibition of mTOR, a kinase involved in several biological processes, improves the response of memory CD8 T-cells.

Susceptibility to oil spill spreading using case studies and simulated scenarios.

Fossil fuels still prevail over other energy sources in the world's consumption energy matrix. Thus, oil transportation and operations over maritime routes have been in high demand for a long time. Although oil spill accidents caused by these activities have reduced significantly over the last few decades, they still cause great concern.

Integrated environmental vulnerability to oil spills in sensitive areas.

As the typical range of influence of oil spills surrounds urbanised and economically active areas, it is likely that fragile regions may not be part of the most vulnerable zones. This premise is remediated in this paper with the adoption of a vulnerability approach based on the integration of static and dynamic information, such as oil pollution susceptibility. Susceptibility is a poorly consolidated term and is often used as synonym for environmental sensitivity; it is considered here to be the distribution areas of oil slicks.

LFA-1 Mediates Cytotoxicity and Tissue Migration of Specific CD8 T Cells after Heterologous Prime-Boost Vaccination against Infection.

Integrins mediate the lymphocyte migration into an infected tissue, and these cells are essential for controlling the multiplication of many intracellular parasites such as , the causative agent of Chagas disease. Here, we explore LFA-1 and VLA-4 roles in the migration of specific CD8 T cells generated by heterologous prime-boost immunization during experimental infection with . To this end, vaccinated mice were treated with monoclonal anti-LFA-1 and/or anti-VLA-4 to block these molecules.