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By Frank J. Dixon, K. Frank Austen, Leroy E. Hood, Jonathan W. Uhr (Eds.)

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The demonstration that the IgD- B cells were enriched in cells responding to T cell factors alone or PWM in the presence of T cells and the finding that they were also enriched for postswitch precursors of IgG- and IgAsecreting cells indicate that they were a more mature subset of B cells. Heterogeneity in the degree of activation could be found in the IgDpopulation. Thus, both a resting 4F2- and an activated 4F2+ B cell were found in the IgD- subset. Removal of the activated 4F2+ B cells still permitted IgM, IgG, and IgA secretion, supporting the conclusion that the IgD- population contained a subset of resting memory B cells.

The product of this cDNA was found to support the proliferation of human T cells and helper T cell clones as well as the proliferation of anti-IgM-activated human tonsillar B cells and thus is similar to murine BSF-1. However, it has not yet been determined whether the human BSF-1 equivalent has an effect on IgGl and IgE production or on class I1 MHC antigen expression. Of further interest was the finding by these investigators that B LYMPHOCYTE ACTIVATION 31 proliferation of anti-IgM-stimulated B cells was supported by either cloned BSF-1 or a commercially available preparation of BCGF, whereas SA-stimulated B cell proliferation was supported only by the BCGF preparation.

44 DIANE F. JELINEK AND PETER E. LIPSKY was somewhat less active than r-IL-2. r-IFN-y, however, was unable to promote differentiation of activated B cells into Ig-secreting cells during the terminal incubation even when T cell supernatant had been present during the initial activation period. By contrast, r-IL-2 was not only effective at promoting the generation of Ig-secreting cells following activation with SA + T cell supernatant but it also supported the generation of Ig-secreting cells from B cells initially activated with SA + r-IL-2, thus indicating that IL-2 alone could function as a B cell differentiation factor.

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