Thymus Dependence of Resistance to Infection with Babesia microti of Human Origin in Mice

Abstract

The nature of resistance to a primary infection with Babesia microti (Peabody strain) was studied in lethally irradiated, bone marrow- and/or thymocyte-reconstituted BALB/c mice. Mice depleted of T lymphocytes by thymectomy, lethal irradiation, and reconstitution with anti-theta serum-treated bone marrow cells developed significantly higher parasitemias than sham-thymectomized, lethally irradiated mice reconstituted with thymocytes alone. Natural resistance to B. microti could be partially restored to T lymphocyte-depleted mice by transfer of spleen cells depleted of B lymphocytes by treatment with anti-immunoglobulin serum. The greatest resistance to infection among lethally irradiated mice, however, was observed when T lymphocytes were given to mice with intact thymuses. The return of the spleen to normal size after enlargement resulting from infection with B. microti was shown to be a T cell-mediated response. Twenty days after peak parasitemia, the total cell and leucocyte numbers in the spleens of mice depleted of T lymphocytes were considerably higher than those of mice given T cells. A depression of humoral immune responsiveness to sheep red blood cells was also noted during primary B. microti infection, while cell-mediated immune responses remained near normal. Although the mechanism of parasite destruction was not determined, these results suggest that resistance to and recovery from a primary B. microti infection is modulated by T lymphocytes, and that depressed B cell function and normal T cell function are correlates of this infection.