Contribution of B-1 cells in the cytotoxicity of CD8 T lymphocytes in encephalitozoonosis

Abstract

Encephalitozoon cuniculi is an opportunistic intracellular pathogen that establishes a balanced relationship with immunocompetent individuals depending on the activity of their CD8+ T cells lymphocytes. However, lower resistance to experimental infection with E. cuniculi was found in B-1 deficient mice (Xid), besides increased the number of CD8 T lymphocytes. Here, we evaluated the cytotoxic activity of CD8+ T lymphocytes from Balb/c wild-type (WT) or Balb/c Xid mice (with B-1 cell deficiency) on the microbicidal activity of macrophages challenged with E. cuniculi. CD8 T lymphocytes from WT or Xid mice previously infected or not with E cuniculi were co-cultured with macrophages challenged with E. cuniculi. We evaluated macrophages viability and microbicidal activity, and proliferation, viability, and presence of activating molecules (CD62L, CD69, and CD107a) in CD8 T lymphocytes. Macrophages co-cultured with CD8 T lymphocytes from WT demonstrated high microbicidal activity. CD8 T lymphocytes obtained from uninfected WT mice had a higher proliferative capacity and a higher expression of CD69 and LAMP-1-activating molecules compared to Xid CD8+ T lymphocytes. CD8 T lymphocytes from infected Xid mice proliferated more than those from WT mice, however, when the expression of the activating molecule CD69 associated with the expression of CD62L was kept low. In conclusion, the absence of B-1 cells in Xid mice might be associated with the lower expression of activating molecules in CD8+ T lymphocytes and their cytotoxic activity. However, after a previous infection with E. cuniculi, CD8 T lymphocytes were more effective in killing macrophages infected with E. cuniculi.