X-linked recessive inheritance of a defective responsiveness to T-cell-replacing factor in DBA/2Ha mice.

TRF responsivity of B-cells from an F1 hybrid of the low-responder strain DBA/2Ha (female) and the high-responder strain BALB/c (male), or their reciprocal F1 hybrid (BALB/c (female) X DBA/2Ha (male)), was analyzed. In every case the B-cells from all of the male mice of the (DBA/2Ha X BALB/c) (DC)F1 hybrid were incapable of responding to TRF, whereas B-cells from female mice of the same litter responded to TRF. In contrast, B-cells from both male and female (BALB/c X DBA/2Ha) (CD)F1 mice were able tp respond to TRF, strongly suggesting that the responsivity of B-cells to TRF is controlled by the X-chromosome of the high-response animals. To substantiate further the evidence for a X-linked B-cell defect in DBA/2Ha mice, we analyzed TRF responsivity of B-cells from back-cross (DCF1 (female) X DBA/2Ha (male)) progeny and from F2 (DCF1 X DCF1) progeny, respectively. In both crosses we observed segregation of TRF responsivity into high-responder and low-responder groups in a nearly 1:1 ratio. These findings further indicated that a major component involved in the regulation of TRF responsivity is carried on the X-chromosome. This component is defective in DBA/2Ha mice, the defect being inherited in a recessive manner.