By Maureen Howard

نویسندگان

  • MAUREEN HOWARD
  • STEVEN B. MIZEL
  • LAWRENCE LACHMAN
  • JOHN ANSEL
  • BARBARA JOHNSON
  • WILLIAM E. PAUL
چکیده

The use of anti-Ig antibodies to stimulate polyclonal proliferation through Ig receptors expressed on the B cell membrane has been a popular model for antigendriven B cell activation (1-7). Initially it was proposed that anti-Ig-induced proliferation proceeded independently of T cells and other accessory ceils, as vigorous depletion of such cell types failed to prevent activation (3, 8). However, certain features of anti-Ig-induced B cell activation challenged the view that the response was a simple consequence of the interaction of anti-Ig and membrane Ig. In particular, the relationship between cell density and magnitude of the proliferative response was nonlinear and rapidly declined to background proliferation levels at cell numbers below 105 per microtiter well (3, 6). Furthermore, the opt imum doses of anti-Ig used in such studies far exceeded the amount required to saturate membrane Ig receptors and induce capping of membrane components. Precise delineation of the stimuli required for anti-Ig-induced B cell activation requires a functional assay in which contaminat ing accessory cells potentially capable of endogenous factor production have been excluded. To this end, we have investigated conditions required for polyclonal activation of highly purified mouse B lymphocytes cultured at low cell density (e.g., 5 × 104 cells/well). Using such an assay, we have shown the role of a T cell-derived factor, designated B cell growth factor (BCGF), 1 in anti-IgM-induced B cell proliferation. (9). In this report we demonstrate that in the presence of opt imum amounts ofBCGF, anti-IgM-induced proliferation of B cells cultured at lower densities (1-2 × 104 cells/well) is enhanced by the addition of a second soluble factor. Biochemical analyses identify this second cofactor as the previously described monokine interleukin 1 (IL-1).

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تاریخ انتشار 2003