Thymic atrophy induced by Plasmodium berghei ANKA and Plasmodium yoelii 17XL infection.

• Malaria infection leads to the development of thymic atrophy. • Thymic atrophy does not depend on parasitemia level but on the specific host-parasite interaction. • Thymus atrophy seems to be associated with a corticosterone-induced effect and had no association with elevated serum cytokines levels. • The severity of thymic damage in both malaria models reached the same extent, although it occurs at different stages of infection. The thymus is the anatomical site where T cells undergo a complex process of differentiation, proliferation, selection, and elimination of autorreactive cells which involves molecular signals in different intrathymic environment. However, the immunological functions of the thymus can be compromised upon exposure to different infections, affecting thymocyte populations. In this work, we investigated the impact of malaria parasites on the thymus by using C57BL/6 mice infected with Plasmodium berghei ANKA and Plasmodium yoelii 17XL; these lethal infection models represent the most severe complications, cerebral malaria, and anemia respectively. Data showed a reduction in the thymic weight and cellularity involving different T cell maturation stages, mainly CD4−CD8− and CD4+CD8+ thymocytes, as well as an increased presence of apoptotic cells, leading to significant thymic cortex reduction. Thymus atrophy showed no association with elevated serum cytokines levels, although increased glucocorticoid levels did. The severity of thymic damage in both models reached the same extend although it occurs at different stages of infection, showing that thymic atrophy does not depend on parasitemia level but on the specific host-parasite interaction. [ABSTRACT FROM AUTHOR]