The affinity of serum antibodies produced by selectively bred lines of mice [high affinity, low affinity, low nonmaturing (N/M)] injected with T-dependent [human serum albumin (HSA), dinitrophenylated bovine gamma-globulin (DNP-BGG)] and T-independent (DNP-Ficoll) antigens in saline and adjuvant has been determined. The lines of mice differ significantly in the affinity of antibody produced to T-dependent antigens injected in saline but not to the T-independent antigen. Unlike mice of the high and low-affinity lines, low-affinity N/M mice failed to show affinity maturation to HSA and DNP-BGG injected in Freund's incomplete adjuvant. However, low-N/M mice responded to DNP-Ficoll injected in adjuvant by the production of antibody of affinity comparable to that produced in the other lines and with a similar maturation in affinity. Carrier priming resulted in the suppression of anti-hapten antibody affinity in all lines but low-N/M mice showed significantly greater suppression late in the response to challenge. Low doses of cyclophosphamide produced a significant increase in affinity in low-N/M mice. These results suggest that the failure of low-N/M mice to show affinity maturation results from increased suppressor T cell activity. The availability of the selectively bred mice provides a useful model for the detailed study of the cellular basis of the control of antibody affinity maturation.
Whereas it is generally believed that most cases of hairy cell leukaemia (HCL) represent B cell neoplasms, it is reported here that 4 of 14 cases of HCL not only express monotypic surface immunoglobulin (SIg) but also react with the T cell‐specific monoclonal antibody (Mab) UCHT1 by indirect immunofluorescence or immunoperoxidase staining. Although both UCHT1 and OKT3 recognize the T3 molecule, which is expressed in all normal T cells, UCHT1+ hairy cells (HCs) were consistently OKT3−. Spurious reactivity of UCHT1 antibodies with SIg+ HCs was excluded by showing that lymphocytes sensitized with an irrelevant mouse Mab did not stain with second layer antibodies and lymphocytes sensitized with second layer antibodies alone were always completely unreactive. Moreover, in 1 case the determinants demonstrable by both UCHT1 and anti‐Ig were strongly re‐expressed after capping and shedding, i.e. appeared to be endogenous. It is concluded that HCs with a hybrid T‐B surface phenotype are more common than hitherto reported, that HCs may express T3 molecules as well as SIg but that determinants recognized by OKT3 may be cryptic or buried in the HC membrane.
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