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Activation of T lymphocytes by lectins and carbohydrate‐oxidizing reagents viewed as an immunological recognition of cell‐surface modifications seen in the context of “self” major histocompatibility complex antigens

The experiments reported here were directed at the question of whether polyclonal activation of T cells by mitogenic substances results as a consequence of (a) a truly antigen‐independent stimulation of T cells through mitogen receptors, bypassing requirements for T cell‐specific recognition or (b) an immunological reaction, similar in principle and requirements to T cell activation induced by antigen. Several lines of evidence have provided strong support for the latter interpretation. First, the ability of several mitogenic substances to induce polyclonal T cell activation was found to be crucially dependent upon cell surface expression of major histocompatibility complex (MHC) products. Thus, the presence of alloantisera or monoclonal antibodies directed against either class I (SD) determinants or class II (Ia) products on the responding cell population resulted in a sizeable dose‐dependent inhibition of the mitogenic response. Additional studies using spleen cells from normal F1 mice or F1→parent bone marrow chimeras provided the most direct and convincing evidence for a specific immunological role of MHC products in mitogenic T cell activation. Here, the concanavalin A response of normal F1 T cells was found to be inhibited by alloantisera against either parental haplotype, while the H‐2‐heterozygous F1→parent chimeras were only inhibited by antisera against the H‐2 of the parent in which they matured and possessed functional, MHC‐restricted helper T cells.