Ontogeny of B lymphocyte function X. Strain differences in maturation of the capacity of the B lymphocyte population to produce a high‐affinity antibody response

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Abstract
The ontogeny of the B lymphocyte population to be capable of producing a high‐affinity plaque‐forming cell (PFC) response to a haptenic determinant was studied by cell‐transfer techniques in five different mouse strains. Lethally irradiated adult mice were reconstituted with liver from fetal or neonatal donors or spleen from young donors as a source of B lymphocytes. In addition, all animals received 1 × 108 adult thymus cells. Recipients were immunized with dinitrophenylated bovine gamma‐globulin (DNP‐BGG) one day after cell transfer. The heterogeneity of affinity of their anti‐DNP PFC response was assayed by hapten inhibition of plaque formation. It was established by use of congenic mice differing at the Igh locus that only donor cells responded under these conditions. By use of this transfer system, it was shown that the B cell populations of A/HeJ, AKR and C57L/J mice aquire the capacity to produce a high‐affinity PFC response between day 15 and 18 of fetal life. The B cell populations of LAF1 and DBA/1 J mice mature between 7 and 10 days after birth. The B cell population of C57BL/6 J mice matures between 21 and 28 days of age. In LAF1 and AKR mice, the B cell population acquires the capacity to generate a high‐affinity indirect PFC response at approximately the same time as the capacity to generate a high‐affinity direct PFC response. The time of maturation of the capacity to generate indirect PFC was found to differ in different strains of mice. Maturation of the capacity to produce indirect PFC appears to represent a dinstinctly different differentiation event from the acquisition of the capacity to produce a high‐affinity PFC response. The data suggest that the maturation of the B cell population to be capable of producing high‐affinity PFC is a precisely regulated differentiation event, the timing of which is strain‐related. Preliminary data suggest that this regulation is not linked to either the H‐2 haplotype or to the Igh allotype.