SOLITON GROWTH-SIGNAL TRANSDUCTION IN TOPOLOGICALLY QUANTIZED T-CELLS

A model for growth-signal transduction of the T cell and its growth fa ctor, interleukin-2, is presented. It is obtained as a generalization of the usual rate equation and is founded on the observation that a de finite number of receptor occupations must take place in order to prom ote transition to the S phase and subsequent DNA replication. The gene ralized rate equation is identified as the equation of motion of a Lag rangian field theory of Ginzburg-Landau (Goldstone) type. However it i s not an ad hoc model but is a microscopic theory of the interaction o f interleukin-2 and its receptor. The topological quantum number of th e model is related to the observed definite number of receptor occupat ions required to elicit growth-signal transduction. Individual recepto r quanta, up to this limit, are subjected to a type of Bose condensati on. This collective excitation constitutes the growth signal in the fo rm of a topological kink soliton which is then launched by the next po tential receptor occupation that makes the interaction repulsive. The model provides a possible long-absent explanation of the triggering me chanism for growth-signal transduction by means of the ambivalent inte raction, which switches sign after a definite number of receptor occup ations. Moreover, it offers an explanation of how Nature screens out f ractional signals in the growth-signal-transduction process of T cells . Although the model is derived for assumed point-like cells and certa in other restrictions, the obtained dose-response curves are in striki ng agreement with proliferation data from studies of both the leukemic T cell line MLA-144 from gibbon ape and normal human T cells in, and without, the presence of monoclonal anti-Tac antibodies.