Interleukin-2 Receptors on Activated Malignant and Normal B-Cells

Abstract

A battery of antigen non-specific, genetically unrestricted factors derived from T cells have been shown to play a role in the regulation of B-cell responses (Howard and Paul 1983). One such factor designated B-cell growth factor (BCGF) appears to be required for the proliferation of a subset of B cells following their interaction with antigen or with anti-immunoglobulin molecules. A second set of factors termed B-cell differentiation or T-cell replacing factors (TRF) is involved in the terminal maturation of such proliferating B-cells into immunoglobulin secreting cells. There has been controversy concerning the possible involvement of T-cell growth factor or interleukin-2 (IL-2) in B-cell responses and concerning the ability of this growth factor to act directly on B lymphocytes. The proponents of a direct action of IL-2 on B-cells have shown that depletion of IL-2 from cofactor rich supernatants by absorption on IL-2 dependent T-cell lines also removes a factor required for B-cell differentiation (Parker 1982; Leibson et al. 1981). The view that IL-2 acts directly on B-cells has been challenged since the IL-2 containing supernatants generally used in the previous studies also contained BCGF and one or more TRF’s (Howard and Paul 1983). Furthermore, IL-2 was not absorbed by resting B-cells, LPS stimulated splenic lymphoblasts or by either of the two Burkitt’s lymphoma B-cell lines examined suggesting that B-cells do not manifest receptors for IL-2 (Robb et al. 1981).