T lymphocyteB lymphocyte interaction

The first experiments to demonstrate directly the failure of cooperation of histoincompatible T and B lymphocytes to generate an antibody response were performed by Katz and coworkers. In these studies, F1 recipients were injected with carrier primed T cells from one of the parental strains, irradiated 24 h later, and then injected with B lymphocytes from the other parent primed to a hapten on a heterologous carrier. The reconstituted animals were then immunized with the appropriate hapten-carrier conjugate and the antihapten response was measured 7 days later. If the carrier-primed T lymphocytes and hapten-primed B lymphocytes were derived from the same parental strain, an antihapten antibody could be measured. The failure of histoincompatible helper T lymphocytes to collaborate with hapten-specific B lymphocytes was not secondary to an 'allogeneic effect' because B lymphocytes derived from Fl animals could cooperate with T lymphocytes derived from either parental strain; presumably, under these latter conditions, the interaction of parental strain T lymphocytes with Fl B lymphocytes would have been accompanied by as great an 'allogeneic effect' as that seen when T and B lymphocytes from MHC incompatible strains were used. Detailed genetic mapping studies demonstrated that the genes which controlled T lymphocyte/B lymphocyte interaction also mapped to the I-region of the MHC.

One of the major problems in the analysis of MHC restriction on T/B interaction resulted from the demonstration that macrophage/T lymphocyte interaction is restricted. It is therefore possible that the observed restriction on T/B interactions was secondary to a restriction on macrophage/T lymphocyte interaction which occurred early in the priming of the helper T lymphocyte. In order to resolve the issue of whether macrophage/T cell interaction controls the subsequent ability of primed T helper cells to interact with B cells, Fl T cells were primed in vitro with parental strain macrophages and then tested for their ability to collaborate with B cells syngeneic to the macrophage donor or with B cells derived from the other parental strain. Unfortunately, this experimental protocol resulted in conflicting results when performed in multiple independent laboratories. In some cases, restriction could only be observed at the level of macrophage/T cell interaction, with T/B interaction completely unrestricted, while in other studies clear-cut restrictions in both interactions were documented. The solution of this dilemma required the use of T cell clones and an in-depth analysis of the heterogeneity of the responding B cell population. Thus, there appear to be two distinct B

cell populations which are capable of interacting with primed T helper cells. One population can interact with histoincompatible helper T cells, requires only T cell-derived growth factors, high concentration of antigen, produces mainly IgM antibody, and does not require that the hapten and carrier be linked. In contrast, a second population of B cells requires genetically restricted T cell help, needs only low concentrations of antigen to differentiate into a plasma cell, produces mainly IgG antibody, and requires that the hapten and carrier molecules be linked.

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