Regulation of human B cell activation and antibody production by non‐major histocompatibility complex‐restricted cytotoxic T lymphocytes

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Abstract
To determine whether non‐major histocompatibility complex‐restricted cytotoxic human T lymphocytes (NrCTL) are involved in the regulation of antibody response, we studied the effect of a CD3, T cell receptor (TcR)‐α/β, NKH1 clone named JT9 on B cell proliferation and differentiation. It was found that low amounts of JT9 clone (5%) profoundly inhibited (> 80%) in vitro specific anti‐trinitrophenyl primary antibody response. This inhibition did not need the presence of autologous T cells and took place at the induction phase of the antibody response. JT9 clone had no effect on resting B cells but enhanced proliferation of anti‐μ‐stimulated B cells. Respective involvements of cell to cell interaction, cytotoxicity and lymphokines were investigated. (a) The effect of monoclonal antibodies (mAb) inhibiting cytotoxic properties of JT9 clone, i.e. an anti‐clonotypic structure mAb and a mAb directed against a target cell antigen similar to 4F2, were studied. These mAb did not reverse the effects of JT9 on B cell activation and differentiation. Thus, these contrasting effects of JT9 clone on B cell response did not seem to involve an interaction of JT9 clone TcR with its target or, further, cytotoxic properties for which this clone had been characterized. (b) Supernatant of JT9 clone stimulated by cross‐linking of TcR complex, in the absence of interleukin 2, exerted a proliferative effect on anti‐μ‐stimulated B cells but not on resting B cells. These findings suggest that JT9 clone could secrete a B cell growth factor – like activity and that NrCTL cells may play an important role in the regulation of antibody response.

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