ACOSTA RODRÍGUEZ EVA VIRGINIA
Congresos y reuniones científicas
Título:
Study of the role of tissue resident regulatory T cells during Trypanosoma cruzi infection.
Autor/es:
BOCCARDO S; ARAUJO FURLÁN CL; RODRIGUEZ C; ALMADA L; ABRATE C; MONTES CL; GRUPPI A; ACOSTA RODRIGUEZ EV
Reunión:
Congreso; Reunión Conjunta de Sociedades de Biociencias; 2017
Resumen:
Tissue resident CD4+Foxp3+ regulatory T cells (tTregs) haveemerged as a specialized Treg subset that exhibit phenotypic, functional and transcriptional profiles particular to each tissue. tTregs notonly regulate immune effector function as lymphoid Tregs but alsomodulate several non-immune biological processes and maintaintissue homeostasis. T. cruzi (Tc) triggers a strong effector responsethat controls parasite spreading and may promote tissue damageand immune pathology. Our previous results showed that Tc infectionis linked to a limited Tregs response that is required for theemergence of protective CD8+ T cell immunity.Our current aim is to evaluate whether tTregs plays any role in theregulation of tissue damage and pathogenesis in Chagas disease.To this end, Foxp3-GFP C57BL/6 mice were infected with 5000 Tcparasites (Tulahuen) and frequency and phenotype of Tregs weredetermined by flow cytometry in blood and spleen as well as in targettissues such as liver (L), skeletal muscle (SM) and heart (H) atdifferent days post-infection (dpi). As reported in blood and spleen,the frequency of Tregs identified as CD4+Foxp3-GFP+ T cells decreasedin L, SM and H along the infection. We next evaluated theexpression of IL-18R and ST2, required for survival and consideredmarkers of tTregs. Tc infection did not change the % of either IL-18R+ Tregs in any organ or ST2+ Tregs in spleen but it reduced %of ST2+ Tregs in L and SM. Finally, we studied whether Tc infectiontriggered the production of tTregs growth factors such as IL-33. Wedetermined by ELISA that while IL-33 was detectable at low concentrationin the plasma of non-infected mice, it became undetectableafter 14 and 21 dpi (p<0.001). Our preliminary results suggest thattTregs are not induced during Tc infection and this may be associatedto a greater damage in target organs. Further studies mayestablish whether boosting tTregs generation may be useful to limitimmunopathology during Tc infection.