B-cell transplants to immunodeficient xid neonates do not imprint their helper T cells.

A great variety of Igh-restricted immunoregulatory phenomena have been described in responses to both haptens and carriers. The investigation of Igh-dependent T-cell functions is of considerable interest because it relates to issues such as the interdependence of the T- and B-cell networks, isotope- and idiotype-specific help, the role of Igh-linked products in the generation of the helper and cytolytic T-cell repertoires and Igh-linked effects on cell interactions among helper and suppressor cells. Helper T cells have been shown to be critically susceptible to B cell-mediated education and it is generally assumed that T cells become imprinted by B-cell idiotypes during development. It occurred to us that xid immunodeficient neonates, which lack T15+ B cells and T15 antibodies, might provide a suitable host to investigate the B-cell dependent imprinting of T cells providing help in T15+ anti-PC responses. We designed our experiments to test whether or not T15 deficient xid mice could be used as recipients of normal B cells capable of imprinting the host's helper cells. The results of our experiments demonstrate that unirradiated xid neonates are readily engrafted with normal B cells from both neonatal and adult donors. The transplanted B cells reconstitute anti-PC and anti TNP-FICOLL PFC responses in the xid hosts. However, the early engraftment of T15+ B cells in xid mice did not cause a detectable imprinting of their helper T cells, i.e., we could not detect any biases in the preference of carrier-/primed cells from reconstituted mice for primary or secondary T15+ or T15- B cells.(ABSTRACT TRUNCATED AT 250 WORDS)