Profile of T and B lymphocytes in individuals resistant to Schistosoma mansoni infection

Abstract

The mechanisms involved in the development of resistance to infection/reinfection by Schistosoma mansoni still arouse great interest and controversy. Some authors demonstrate that resistance to infection is attributed to a mixed Th1 and Th2 response and resistance to reinfection after repeated treatments through mechanisms associated with the Th2 response. Through flow cytometry, the phenotypic characterization of B and T lymphocytes in individuals residing in endemic areas with low parasite loads over 10 years was evaluated for the first time in humans. In this study, individuals with low parasite loads for Schistosoma mansoni had a higher proportion of Th1 and Th2 cells. In addition, lymphocytes from these individuals showed a higher degree of expression of costimulatory molecules CD28 and CTLA-4 and regulatory molecules FoxP3 and IL-10, when compared to individuals with high parasite loads. Our data indicate that the control of the parasite load of S. mansoni must be associated with a Th1, Th2, and regulatory response, and that further studies are needed to elucidate the possibility of mechanisms associated with the hyporesponsiveness of lymphocytes from individuals with high parasite loads.

Evaluation of IL-35, as a Possible Biomarker for Follow-Up after Therapy, in Chronic Human Schistosoma Infection

“…The exact phenotype of the induced response depends on a complex immunological “dialogue” involving cytokines and immune cells. During infection, the Th1/Th2 responses and the immune-modulating activities by regulatory T (Treg) and B (Breg) cells reflect the interaction between the host immune system and the development of the parasite inside the host, with Th1 (pro-inflammatory) responses (production of IFN-γ, TNFɑ, IL-6, and IL-1) prevailing in the initial acute phase, followed by a Th2 response stimulated by egg antigens and characterized by the production of IL-4, IL-5, IL-13 and IL-10 [ 9 , 10 , 11 ]. The Th2 response regulates Th1-mediated immunopathology and exerts anti-inflammatory effects.…”