Abstract We have made a comparative study of the capacity of normal B cells, B lymphoma cells, and splenic macrophages to present the antigen KLH, either to a KLH-specific, MHC-restricted hybridoma or to KLH-primed normal T cells. Antigen presentation was measured by the capacity of these potential accessory cells together with antigen to stimulate IL 2 production by the T cells. Whereas both the B lymphoma cells and spleen macrophages were effective at presenting antigen, normal B cells were either completely unable or at best highly inefficient in this regard. For example, in the presence of antigen as few as 500 B lymphoma cells were capable of stimulating the T cell hybridoma to produce IL 2, whereas the minimum number of normal B cells capable of causing the same stimulation was 50,000. In contrast to this inefficiency of normal B cells to present antigen was the finding that LPS-stimulated lymphoblasts were as efficient as the B lymphoma cells in presenting antigen. These data suggest the differentiative state of the B cell plays a critical role in determining its capacity to serve as an antigen-presenting cell. We investigated one possible mechanism to explain the inability of resting B cells and the ability of activated B cells and B cell lymphomas to present antigen; i.e., the relative ability of these cells to take up antigen. Fluid phase pinocytosis and binding of antigen to the cell surface were evaluated. The fluid phase pinocytic rate of normal B cells was only 10% that of the B lymphoma cells. Similarly, resting B cells had only 10% of the binding capacity for antigen as the B lymphoma cells or LPS-stimulated lymphoblasts. Although other possible mechanisms exist, these data suggest that differences in the capacity of B cells to take up antigen may be a factor that limits their capacity to serve as antigen-presenting cells.

Chesnut, R. W., Colon, S. M., & Grey, H. M. (1982). Antigen presentation by normal B cells, B cell tumors, and macrophages: functional and biochemical comparison. The Journal of Immunology, 128(4), 1764–1768.