Chronic suppression of immunoglobulin allotype production in adult congenic mice.

Abstract

MOUSE allotypes refer to the inheritance of antigenic differences on the constant region of immunoglobulin (Ig) heavy chains (CH). As such, allotypes are used as genetic markers to distinguish allelic CH genes, the expression of which is codominant in heterozygous mice1,2. The expression of a paternal CH gene, however, can be suppressed in heterozygote offspring if the mother has previously been made immune to the allotype encoded by the paternal gene3. Neonatally induced suppression of this sort is known to lead to (or result in) the generation of allotype-specific suppressor T lymphocytes which directly or indirectly prevent allotype production by B lymphocytes4–6. In contrast to this we have shown that allotype suppression can also be initiated in adult mice, that is in BALB/c mice that are congenic for the C57BL allotype (C.B-17 mice)1. When X-irradiated C.B-17 mice (550 r.) are injected with thymocytes from BALB/c donors immune to the C57BL allotype, IgG2a allotype production in the C.B-17 recipients becomes chronically suppressed7. We now report that allotype suppression in C.B-17 mice is mediated by T cells; that production of only the IgG2a class allotype (G2) is suppressed, presumably as a result of direct interaction between specific T and B cells, and that the capacity of spleen cells to suppress host allotype production can be transferred serially from one C.B-17 mouse to another and as yet without obvious limit.