Inclusion of non-target antigen in vaccination favors generation of OVA specific CD4 memory T cells.

Inducing long-lived memory T cells by sub-unit vaccines has been a challenge. Subunit vaccines containing single immunogenic target antigen from a given pathogen have been designed with the presumption of mimicking the condition associated with natural infection, but fail to induce quality memory responses. In this study, we have included non-target antigens with vaccine candidate, OVA, in the inoculum containing TLR ligands to suffice the minimal condition of pathogen to provoke immune response.

Developing effective vaccines: Cues from natural infection.

The ultimate goal of any vaccine is to generate a heterogeneous and stable pool of memory lymphocytes. Vaccine are designed with the hope to generate antigen specific long-lived T cell responses, as it may be the case in natural infection; however, inducing such response by sub-unit vaccine has been a challenge. Although significant progress has been made, there is lot of scope for designing novel vaccine strategies by taking cues from the natural infection.

Infectious Sporozoites of Effectively Activate Liver CD8α Dendritic Cells.

Immunization with radiation-attenuated sporozoites (RAS) shown to confer complete sterile protection against liver-stage (LS) infection that lasts about 6 to 9 months in mice. We have found that the intermittent infectious sporozoite challenge to immune mice following RAS vaccination extends the longevity of sterile protection by maintaining CD8 T cell memory responses to LS infection. It is reported that CD8α dendritic cells (DCs) are involved in the induction of LS-specific CD8 T cells following RAS or genetically attenuated parasite (GAP) vaccination.

Lack of TNF-α signaling through p55 makes the mice more susceptible to acute infection but does not alter state of latency and reactivation of HSV-1.

TNF-α has been shown to play an important role in pathogenesis and latency of HSV-1 infections. TNF-α signals through TNFR1 (p55) and TNFR2 (p75), and signaling through p55 generally results in gene activation leading to induction of inflammatory responses. Here, we studied the role of TNF-α signaling in latent virus reactivation in p55-knock out (KO) mouse model of ocular HSV-1 infection.