CONICET | Buscador de Institutos y Recursos Humanos

Our previous work demonstrated that during the acute phase of Trypanosoma cruzi infection, where a strong Th1 immune component is present, mature peripheral cells that express CD44, a marker of activated or memory T cells, are able to re-enter the thymus. Our recent immunofluorescence analysis demonstrated that CD44+ T cells in the thymus localized both in the thymic medullary and cortical areas.Besides, under this infectious process, we have observed that CD4+ and CD8+ simple positive (SP) thymocytes adopt a phenotype similar to mature T cells that localize in secondary lymphoid organs (SLO), based on the expression of the markers Qa2 and CD24 evaluated by flow cytometry (inmature: Qa2lo CD24hi more mature: Qa2hi CD24lo). Moreover, recent studies in our group, using intrathymic staining with eFLUOR dye,suggested that conversion to a more mature phenotype occur mainly in the resident CD44lo SP thymocytes in T. cruzi infected mice (control vs infected, p≤ 0,05). Interestingly, our recent finding revealed that early after Candida albicans infection (control vs infected, p≤ 0,05) or after systemic expression of IL-12 or IL-18 by hydrodynamic expression of their cDNAs (control vs treated, p≤ 0,05), SP CD44lo thymocytes also acquired a more mature phenotype similar to what we reported for T. cruzi infection. The latest data let us to hypothesize that a Th1 cytokine inflammatory process rather than a microorganism specific phenomenon is driven this effect. Overall, our data indicate that the thymus is highly susceptible to systemic infectious/inflammatory processes, especially during the acute phase when high levels of IL-12 and IL-18 cytokine are produced. Our data demonstrate that not only peripheral T cell can re-enter the organ in these conditions but also resident SP thymocytes adopt a mature phenotype that would probably alter their own development and future behavior in SLO as T cells.