A cloned, trinitrophenyl (TNP)-specific helper T cell line (TCL), termed E-11, has been established in long-term, interleukin 2-dependent culture and used to study human T helper (Th)-B cell collaboration. Co-culture of E-11 with TNP-modified, but not unmodified or FITC-modified, autologous B cells results in a vigorous, polyclonally plaque-forming cell (PFC) response. E-11 helper activity is not constitutive, but requires antigen-specific, major histocompatibility complex-restricted activation of the TCL cells by interaction with TNP-modified autologous or DR 5+ allogeneic macrophages. Using B cell subsets isolated by discontinuous density gradient cengrifugation as responder populations, we determined that E-11 activates B cell subsets via two distinct mechanisms: (a) E-11 polyclonally activates large B cells in an unrestricted and nonspecific manner; and (b) E-11 preferentially induces a PFC response by TNP-modified small B cells. These results suggest that the large B cell subset is activated by helper signals generated during the Th-antigen-presenting cell interaction, while small B cells require an additional stimulus that is provided by antigen-specific Th-B cell contact.
A cloned major histocompatibility complex-restricted trinitrophenyl-reactive human helper T cell line that activates B cell subsets via two distinct pathways.
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M A Principato, G S Thompson, S M Friedman; A cloned major histocompatibility complex-restricted trinitrophenyl-reactive human helper T cell line that activates B cell subsets via two distinct pathways.. J Exp Med 1 November 1983; 158 (5): 1444–1458. doi: https://doi.org/10.1084/jem.158.5.1444
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