Immunity to Babesia in mice. III. The effects of corticosteroids and anti-thymocyte serum on mice immune to Babesia rodhaini.

BALB/c mice, immunized against Babesia rodhaini by an amicarbalide controlled infection, were exposed to selective immunosuppressive treatment with corticosteroids and anti-thymocyte serum (ATS) respectively. Hydrocortisone acetate, 100 mg/kg, given i.p.

In vitro reactivity to concanavalin A of bovine lymphocytes after cryopreservation.

Cryopreservation of bovine peripheral lymphocytes and its effect on the in vitro response to concanavalin A tested in a microculture system is described. Using DMSO as cryoprotectant in the medium, the cells were cooled to -30 degrees C at 1.3 degrees C/minute and further to -80 degrees C at 6 degrees C/minute and then rapidly to -196 degrees C by dropping in liquid nitrogen.

Immunity to Babesia in mice. II. Cross protection between various Babesia and Plasmodium species and its relevance to the nature of Babesia immunity.

Mice immunized against B. rodhaini by means of a drug-controlled infection were subsequently resistant to infection with B. microti and B.

Immunity to Babesia in mice. I. Adoptive transfer of immunity to Babesia rodhaini with immune spleen cells and the effect of irradiation on the protection of immune mice.

Immunisation of Balb/c mice against Babesia rodhaini by an amicarbalide-controlled infection resulted in a solid immunity which lasted for 216 days. With spleen cells of immune mice protection could be transferred both to naive mice pretreated with cyclophosphamide. Treatment of naive mice with cyclophosphamide (300 mg/kg) five days before a lethal B.

Complement does not play a role in promoting Babesia rodhaini infections in Balb/C mice.

A critical role of C3 and the C3b receptor for the erythrocyte invasion and the development of the parasitemia of B. rodhaini in rats has been described recently (Jack and Ward 1980a). In the present study the influence of the C system on B.