It has long been clear that there are two components of the B cell response to antigen. There is an early phase of proliferation in which the responding B cell population is expanded many times, and a later phase of differentiation in which the already proliferating B cell moves on to the immunoglobulin-secretion stage. It has been suggested that separate signals are involved in each phase (1); it has also been realized that there must be an initial lag phase (2) before the onset of proliferation; more recent studies (3) have defined this activation step as a separate event.It has been many years since the need for a helper T cell in the B cell response to antigen was defined (4, 5) and since the demonstration that the T cell could be replaced by a helper factor (6).It is now known that a number of T cell-and macrophage-derived nonantigenspecific factors make up the activity previously defined as "helper factor." Current studies are underway to characterize each factor and to determine at which stage it acts and what is its exact role. Parker (7) has shown that B cell proliferation can be seen in cultures of positively selected B cells stimulated with anti-#. He showed that anti-# alone was not sufficient, but that interleukin 2-(IL-2) 1 containing supernatants were also required. Immunoglobulin secretion required an additional factor (or factors) not provided in IL-2, but which were present in the supernatant of concanavalin A-(Con A) stimulated T cells. Howard et al. (8; and M. Howard, personal communication) also showed that a number of factors were required for B cell proliferation. In her analysis, the extent of proliferation to anti-Ig was proportional to the third power of the B cell concentration. The slope of this curve was reduced to two by the addition of an IL-2-containing supernatant from EL4 and to nearly one by the further addition of an 18-mol wt cut from the supernatant of P388D1 (presumably, interleukin 1 [IL-1]). The B cell growth factor (BCGF) activity present in the EL4 supernatants could be separated from the IL2 activity by phenyl Sepharose