Following challenge with P. falciparum sporozoite, there was no appreciable effect of vaccination on malaria infection, indicating that multiple immunization and/or higher antibody titers or more robust cellular immune responses are required for protection.
An important goal for human immunodeficiency virus (HIV) vaccines is to develop immunogens that induce broader and more potent cellular immune responses.
The results demonstrated that strong, and compared to protein or DNA vaccination protocols alone, more homogenous, cellular immune responses were induced in cattle vaccinated with the prime-boost regimen.
In pre-clinical comparisons to RTS,S/AS02A in mice and monkeys, RTS,S/AS01B elicited equivalent CSP-specific antibody and greater and more sustained cellular immune responses [14] [16].
However, the use of NYVAC-B-C7L as booster significantly enhanced the magnitude of the T cell responses, and induced a more balanced cellular immune response to the HIV-1 antigens in comparison to that elicited in animals boosted with NYVAC-B.
We previously demonstrated that more effective cellular immune responses are induced with mature DCs compared to immature DCs [ 13].
These results suggest that the BCR/ABL-pIRES-hIL-2 design is capable of inducing a more potent cellular immune response.
Clearly, in our case, this normal antibody response did not prevent the development of persistent C. burnetii infection, as complete clearance might depend more on cellular immune responses.
Our results revealed a significant increase in ConA-stimulated cell proliferation after weaning in piglets of AP sows that may indicate a more effective cellular immune response [ 47, 48].
Histological examination of the abomasal mucosa showed a more pronounced cellular immune infiltration after the primary infection than after the secondary infection.
