Absence of an antigen-specific helper T cell required for the expression of the T 15 idiotype in mice treated with anti-mu antibody.

Abstract

AbstractT‐dependent anti‐phosphorylcholine (PC) plaque‐forming cell (PFC) responses were studied in BALB/c mice. Helper T cells derived from normal, carrier‐primed donors induced anti‐PC PFC responses dominated by the T15 idiotype. Helper T cells derived from carrier‐primed mice that had been treated from birth with anti‐μ antibody, so that they were lacking B cells and circulating antibody bearing the T15 idiotype, also provided helper cell function for the anti‐PC antibody response. In contrast to the response induced by helper T cells from normal mice, T helper cells from μ‐suppressed mice induced an anti‐PC antibody response which was mainly non‐ T15 in character. The failure to induce antibody formation by T15+ B cells was not due to suppressor cells but rather to the lack of an Lyt‐1+ helper T cell population which is necessary for predominant T15 production. This latter cell population was shown to be present in carrier‐primed normal but missing or diminished in carrier‐ primed anti‐μ‐treated BALB/c mice. It required carrier priming for the expression of its helper function, but its function did not require the antigen (carrier) to be physically linked to the hapten. From this, we conclude that dominant production of the T15 idiotype involves the synergistic activity of two antigen‐specific helper T cells. The helper cell population which is required for predominant T15 production is greatly diminished in mice treated with anti‐μ antibody from birth. Hence, the production of circulating T15+ antibody induced by environmental antigens or the appearance of T 15‐bearing B cells would appear to be required for the induction of helper T cells which enhance T15+ anti‐PC antibody synthesis.