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Igh‐1b‐specific CD4+CD8− T cell clones of the Th1 subset selectively suppress the Igh‐1b allotype in vivo

The demonstration of major histocompatibility complex (MHC)‐restricted T helper (Th) cells specific for peptides from the variable (V) regions of syngeneic immunoglobulin (Ig) (idiopeptides) opens the possibility that Th, cells regulate B cell functions via idiopeptide‐based cognate T‐B interactions. As a model for such interactions we investigated the influence of Ig allotype‐specific T cells on the differentiation of H‐2‐syngeneic B cells expressing that particular Ig allotype. We established a BALB/c (H‐2d, Iga) CD4+CD8− T cell line and clones of the Th1 subset (interleukin 2+, interleukin 4−, interferon‐γ+, tumor necrosis factor‐α+) that recognized Igh‐1 (IgG2a) of the b allotype (Igh‐1b) together with I‐Ad. These T cells specifically suppressed surface Igh‐1b+ B cells in vitro and in vivo. In 12 out of 15 6‐week‐old (BALB/c × B10.D2)F1 mice neonatally injected with Igh‐1b‐specific T cells, the serum Igh‐1b concentrations were < 5% of the levels in the controls. Thus, allotype suppression can be accomplished solely by adoptive transfer of Igh‐1b‐specific CD4+ T cells. The in vivo suppression was specific for Igh‐1b+ B cells as the recipients' levels of Igh‐1a and Igh‐4b (IgG1b) were unaffected. The Vβ14‐specific anti‐T cell receptor (TcR) monoclonal antibody 14‐2 inhibited activation of hybridomas derived from two of the clones. Collectively the data indicate that suppression resulted from cognate interactions between allopeptide‐specific TcR α/ß+ T cells and normal unmanipulated B lymphocytes presenting their endogenous Igh‐1b in association with MHC class II molecules. The data support the possibility that normal B cells can be suppressed by idiopeptide‐specific T cells in vivo.