We report here a factor (B cell growth factor) found in induced supernatants of the mouse thymoma EL4 that co-stimulates with anti-IgM antibodies in short-term cultures of purified B lymphocytes to induce polyclonal B cell proliferation but not antibody-forming cell production. The factor is not mitogenic for resting B cells and interacts with anti-IgM-activated B cells in a non-H-2-restricted manner. Absorption studies and molecular weight analysis reveal the factor is distinct from interleukin 2. This factor synergises with antigen, interleukin 2, and an interleukin 2-free, B cell growth factor-free T cell supernatant that contains T cell-replacing factor to produce erythrocyte-specific plaque-forming cells in cultures of highly purified B cells.

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It has been known for over 30 yr that gram-negative bacteria enhance immune responses to vaccines in man (1) and that the active adjuvant component is cell wall lipopolysaecharide (LPS) 1 (2). However, the precise mechanism by which LPS mediates its adjuvant effect has not yet been resolved.Because LPS is a potent B-cell mitogen, a polyclonal B-cell activator, and acts as a T-independent antigen, several investigators have suggested that the adjuvant properties of LPS are most easily ascribed to a direct effect of LPS on the B cells (3-6). Because LPS reverses tolerance to immunity, even in the presence of T-suppressor cells, this has been taken as further proof that LPS enhances B-cell responses (5, 7). LPS can also bypass the requirement for T-helper cells by facilitating immune responses in mice given haptenated, homologous erythrocytes (8, 9). Finally, the lack of tolerance reversal to human gamma globulin by LPS in C3H/HeJ mice (whose B cells are unresponsive to LPS) has been taken as evidence that potentiation is occurring at the level of the B cell (3, 10, 11).Alternatively, a number of studies have suggested that the adjuvant properties of LPS are best explained through activation of T cells (12)(13)(14)(15)(16)(17). Allison and Davies (12), utilizing both thymectomized mice and mice treated with anti-lymphocyte serum, demonstrated that LPS adjuvanticity required normal T-cell populations. In a series of experiments, Katz and coworkers (13-15) also provided evidence for a T-cell requirement during LPS-mediated augmentation of antibody responses. In the first experiments, removal of T cells from antigen-primed spleen cells before adoptive transfer and subsequent challenge abrogated the capacity of LPS to mediate its adjuvant effect (13). Subsequent studies (14, 15) provided evidence that the adjuvant effect of LPS on hapten-specific IgM, IgG, and IgE plaque-forming cell (PFC) responses was exerted on carrier primed, T-helper cell activity. More recent evidence * On sabbatical leave from the

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