Funded by the Royal Society and Hull York Medical School, my laboratory studies B cell and antibody responses to the TriTryp parasites, Trypanosoma cruzi, Trypanosoma brucei and Leishmania spp.
B cells play critical roles in the immune response to the TriTryp parasites. These are kinetoplastid, trypanosomatid protozoan parasites, which are transmitted by insect vectors and cause he TriTryp diseases, Chagas disease, human African trypanosomiasis (HAT) and Leishmaniasis. Together, these diseases affect over 20 million people and cause countless infections in other mammals, primarily in developing countries in tropical and subtropical regions, leading to extensive morbidity and mortality. The TriTryp diseases are part of the 20 World Health Organization's neglected tropical diseases that disproportionately affect the poor. In spite of this large burden and the increasing efforts made by a relatively small group of researchers, no suitable vaccines for these diseases are currently available and treatments are limited to a few drugs that have several undesirable side effects.
The goal of our research programme is to shed light on the mechanisms that regulate B cell responses to TriTryp diseases, and open the door to novel immune therapies and biomarkers to aid in the control of these devastating diseases.
I am an Immunobiologist born and educated in South America, Argentina. I am a Royal Society University Research Fellow, expert in parasitology, B-cell and T-cell biology, both in clinical and experimental settings.
During my postdoc, completed at The Francis Crick Institute (former MRC, National Institute for Medical Research), London, UK, I used mouse models to study the immune response to Plasmodium infection, the cause of malaria, which is among the deadliest infectious diseases worldwide. My research demonstrated the critical role of IL-21 and follicular helper T cells to control and eliminate Plasmodium infection through B-cell responses. In addition, we demonstrated that Plasmodium-specific atypical memory B cells are not that "atypical" or “memory” cells, as they require ongoing subpatent infection to persist, and very similar B cells can be generated by immunizations.
During my PhD, completed at Eva Peron General Hospital and the National Institute of Parasitology, Buenos Aires, Argentina, I studied the immune system of patients with Chagas disease, caused by the protozoan parasite Trypanosoma cruzi infection. Chagas disease is a neglected tropical disease that affect millions of people, primarily economically deprived populations of the Americas. No licensed vaccine is currently available for this disease, and therapeutic drugs are limited and present variable efficacy and undesirable side effects. The lack of early metrics of treatment efficacy and the potential adverse effects of available therapeutics prevent the development of new more efficient drugs and the wide treatment of chronically-infected subjects. We demonstrated that T. cruzi-specific T cell responses represent good surrogate biomarkers of treatment efficacy. With these markers, we showed that treatment with allopurinol combined with benznidazole results in immune changes associated with parasite clearance, and ameliorates the chronic inflammation observed during persistent infection. This resulted in a side project which led us to demonstrate the immunomodulatory effect of allopurinol on human T cells. Finally, we demonstrated the association between different subsets of monocytes with different clinical forms of Chronic Chagas disease.
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