Impact of vaccine stimulation on functionality of antigen presenting cells preconditioned with schistosomal antigens 3728
Abstract Description Helminth infections have been shown to negatively impact vaccine responses to diseases such as tetanus, diphtheria, and influenza. An example of such infection is schistosomiasis, a neglected tropical disease that affects 230 million people globally. During the egg production phase of schistosomiasis, schistosomal egg antigens (SEA) interact with immune cells, such as macrophages, turning them into anti-inflammatory M2 cells. M2 macrophages are antigen presenting cells that interact with naive T-helper cells, which differentiate towards the Th2 response. This Th2 biasing and immune suppression causes some Tc1-dependent vaccines to fail. Listeria monocytogenes encoding an HIV-1 gag sequence generates Tc1 vaccine responses regardless of schistosomiasis status, whereas a DNA-based HIV vaccine (TD158) fails only in mice with chronic schistosomiasis. However, due to the hesitation of using the pathogen L. monocytogenes as a vaccine vector, our work aims to pinpoint the immunological mechanisms of the disparate vaccine responses during chronic schistosomiasis. We expect these insights can be leveraged to develop molecular adjuvants for use in helminth-endemic areas. Here, we are investigating one of the earliest steps in the development of vaccine responses: the interaction of vaccine components with antigen presenting cells, specifically in the context of chronic schistosomiasis, and how these stimulations impact functionality in these cells. Topic Categories Vaccines and Immunotherapy (VAC)
Authors
- Lisa M. Shollenberger (ORCID: https://orcid.org/0000-0002-0943-0838)
- Brent M. Lake
Institutions
- Dominion University College (GH)
- Old Dominion University (US)
Publication Details
- Journal
- The Journal of Immunology
- Published
- 2025-11-01
- DOI
- https://doi.org/10.1093/jimmun/vkaf283.1494
- Primary Topic
- Parasites and Host Interactions
- Type
- article
- Field-Weighted Citation Impact
- 0.00