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

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Extra resources for Advances in Immunology, Vol. 40

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From Jelinek et al. (1986a). B LYMPHOCYTE ACTIVATION 29 presence of T cells but not T cell factors induced 5- to 10-fold greater responses than T cell factors even in the presence of intact T cells. These results support the conclusion that a direct PWM-mediated T cell-B cell interaction is required in these responses. , 1983) although such an interaction is antigen nonspecific and MHC unrestricted. Recent work by Suzuki and colleagues (1986) has shown that the PWM response of human peripheral blood B cells requires at least an initial 6-hour interaction between B and T cells in the presence of monocytes and that this interaction is blocked by the addition of anti-Ia or anti-CD-4 antibodies.

Thus, for example, Kishimoto et al. B LYMPHOCYTE ACTIVATION 35 (1975) demonstrated that the formation or exposure of acceptor sites on B cells for a differentiation factor occurred in the absence of cell division, and therefore likely in GI. Moreover, Miki and co-workers (1982) showed that the signal(s) provided by a T cell-replacing factor to synchronized human B lymphoblastoid cells could be transduced only when cells were in the G1 phase. , 1986). , 1978). , 1983; Hoffmann, 1980b). , 1982). It has been suggested that the primary role of IL-1 is the promotion of activation but, alone, it supports neither growth nor differentiation.

When spleen B cells were examined (Table XV), rIL-2 augmented proliferation of SA-activated B cells just as effectively as T cell supernatant. In contrast to peripheral blood B cells, r-IL-2 was only minimally able to support DNA synthesis by anti-p-activated spleen B cells, whereas T cell supernatant supported substantial DNA synthesis. Analysis of lymph node B cell responses revealed that T cell supernatant supported considerable DNA synthesis by SA and anti-p-stimulated lymph node B cells but IL-2 was considerably less effective in supporting responses by either of the stimuli.

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