Cellular immune response induced by surface immunogenic protein with AbISCO-100 adjuvant vaccination decreases group B Streptococcus vaginal colonization.

Group B Streptococcus (GBS) represents one of the most common causes of bacterial infection in neonates; it is also associated with premature childbirth and stillbirth. A vaccine against GBS is needed, but no approved vaccines are yet available. The Surface Immunogenic Protein (SIP) of GBS is conserved in all serotypes and had been reported to be a good vaccine prototype in a mouse model of GBS infection.

Oral administration of recombinant Neisseria meningitidis PorA genetically fused to H. pylori HpaA antigen increases antibody levels in mouse serum, suggesting that PorA behaves as a putative adjuvant.

The Neisseria meningitidis outer membrane protein PorA from a Chilean strain was purified as a recombinant protein. PorA mixed with AbISCO induced bactericidal antibodies against N. meningitidis in mice.

Role of dopamine in the physiology of T-cells and dendritic cells.

Dendritic cells (DCs) are responsible for priming T-cells and for promoting their differentiation from naïve T-cells into appropriate effector cells. Because of their fundamental roles in controlling immunity, DCs and T-cells require tight regulatory mechanisms. Several studies have shown that dopamine, not only mediate interactions into the nervous system, but can also contribute to the modulation of immunity.

Modulation of nuclear factor-kappaB activity can influence the susceptibility to systemic lupus erythematosus.

Autoimmune diseases, such as systemic lupus erythematosus (SLE), result from deficiencies in self-antigen tolerance processes, which require regulated dendritic cell (DC) function. In this study we evaluated the phenotype of DCs during the onset of SLE in a mouse model, in which deletion of the inhibitory receptor FcgammaRIIb leads to the production of anti-nuclear antibodies and glomerulonephritis. Splenic DCs from FcgammaRIIb-deficient mice suffering from SLE showed increased expression of co-stimulatory molecules.