The immunological response of CBA mice to P. yoelii. II. The passive transfer of immunity with serum and cells.
CBA mice infected with the malaria parasite Plasmodium berghei yoelii (P. yoelii) develop a self-resolving infection lasting 15-18 days; on recovery from a primary infection they are immune to further infection. Cell and serum transfers from immune to non-immune mice were used to analyse the mechanism of resistance. Whereas serum from mice which had recovered from a single infection was ineffective in transferring immunity, hyperimmune serum (from mice repeatedly challenged with P. yoelii) protected against challenge inocula of 10(4) and 5 X 10(4) but was ineffective against higher inocula (10(5)). Doses of serum which completely protected intact mice were ineffective when administered to T-cell deprived recipients. The injection of spleen cells from recovered mice conferred immunity on both normal and T cell deprived mice. Pretreatment of immune cell donors with cyclophosphamide reduce the ability of spleen cells to transfer immunity. Treatment of the immune cells with an anti-Thy 1 antiserum and complement in vitro did not abrogate their protective effect. The significance of these results is discussed in relation to the effector mechanisms which might operate in murine malaria.
D000818:Animals; D003520:Cyclophosphamide / Q000494:pharmacology; D007116:Immunization, Passive; D008212:Lymphocyte Depletion; D008288:Malaria / Q000276:immunology*; D008297:Male; D051379:Mice; D008808:Mice, Inbred CBA / Q000276:immunology*; D010962:Plasmodium berghei / Q000276:immunology; D013154:Spleen / Q000276:immunology / Q000637:transplantation; D013601:T-Lymphocytes / Q000276:immunology
D003520:Cyclophosphamide