Modulation of mouse anti-SRBC antibody responses by placental extracts. II. Antigen specificity and regulatory role of B and T cell populations affected by two distinct placental fractions.

Previous results from our group had shown that when CBA mice are primed to sheep red blood cells (SRBC) in the presence of various doses of placental extract (PE) (or liver extract [LE] as control), their spleen cells injected into normal syngeneic recipients have important immunoregulatory properties. Low doses of PE (0.25 to 4 mg per mouse) induce a marked decrease of the PFC response against SRBC in recipient animals. In contrast, higher doses of PE (8 to 13 mg per mouse) have a potentiating effect on the same response. LE is not different from a saline injection, at any dose. The suppressive and enhancing effects can be reproduced with two distinct placental fractions (PF) of 40 KD and 60 KD, respectively. In the present report, we have studied the requirement for an antigenic stimulation at the same time as the injection of PE, and the antigenic specificity of the subsequent immunoregulatory effects. In addition, we have analyzed the functional properties of the spleen cell populations affected by PE or placental fractions: surface Ig- cells mediate the suppressive effect due to low doses of PE or the 40-KD fraction, whereas surface Ig+ cells are responsible for the enhancing effect due to high doses of PE or the 60-KD fraction. These immunoregulatory activities do not appear to be related to the presence of Ig fragments in PF, because our results have shown that no Ig fragments can be detected in either PF. Surface Ig- T cell populations from spleen cells treated with the 40-KD fraction and antigen have been further separated into Lyt-2- and Lyt-2+ subpopulations. Our results showed that Lyt-2+ cells alone suppress the PFC response anti-SRBC in both normal and irradiated syngeneic recipients. Thus, the injection of a 40-KD PF in the presence of antigen activates splenic T suppressor cells capable of specifically regulating a secondary antibody response in vivo.