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Helminth infections interfere with vaccination efficacy
10th Euro Global Summit and Expo on Vaccines & Vaccination
June 16-18, 2016 Rome, Italy

Minka Breloer

Bernhard Nocht Institute for Tropical Medicine, Germany

Posters & Accepted Abstracts: J Vaccines Vaccin

Abstract:

One third of the human population is infected with parasitic worms. To avoid their elimination, these parasites actively dampen the immune response of their hosts. This immune suppression will also affect immune responses to third party antigens such as vaccines. Accordingly, several studies report a negative correlation between pre-existing helminth infections and response to vaccination in the human population. We use Litomosoides sigmodontis infected mice to further analyze this parasite induced interference with vaccination efficacy. We show that experimental vaccination against the liver stage of Plasmodium berghei elicited reduced numbers of Plasmodium specific CD8+ cytotoxic T lymphocytes in mice with concurrent L. sigmodontis infection. Chronic nematode infection also led to complete suppression of IgG responses to thymus dependent (TD) model antigen vaccinations (DNP-KLH, Ovalbumin). Thereby, the parasite suppressed B-cell function indirectly, via accessory CD4+ T helper cells, as thymus independent vaccination (NIP-Ficoll) was functional and already numbers and frequency of vaccine induced follicular T-helper cells were reduced. Strikingly, a reduced humoral response to TD vaccination was still observed if vaccination was performed more than 16 weeks after clearance of infection. Thus, vaccination may not only fail in helminth infected individuals but also in individuals with a history of previous helminth infections. Helminth induced interference with bystander CD4+T cell activation resulted in a suppressed antigen specific proliferation of Ovalbumin specific TCR transgenic OT-II T cells in vivo, after adoptive transfer into L. sigmodontis infected mice. Using this simplified system, we are currently unraveling the chain of events leading from the presence of L. sigmodontis in the thoracic cavity to the final suppression of T cells specific for a different antigen at a different site.

Biography :

Email: breloer@bni-hamburg.de