LYMPHOCYTE-PROLIFERATION IN MICE CONGENITALLY DEFICIENT IN T-CELL RECEPTOR ALPHA-BETA(+) CELLS

In mice and humans, T cells are characterized on the basis of T-cell r eceptor (TcR) expression and divided into the major TcR alpha beta(+) and minor TcR gamma delta(+) populations, TcR alpha beta(+) cells are considered to be the primary regulators of the immune response, wherea s the function of TcR gamma delta(+) cells is unclear, Mice congenital ly deficient in TcR alpha beta-expressing cells provide an ideal model for analyzing the independent in vivo function of TcR gamma delta(+) cells in the absence of TcR alpha beta(+) cells, Here we report that l ymphoid organs in TcR alpha mutant mice undergo substantial enlargemen t after being challenged by environmental antigens, This organ expansi on can be attributed in part to increases in the relative proportions and absolute numbers of TcR gamma delta(+) cells, but an expansion of the recently described TcR beta(+)alpha(-) population also has a role, The expansion of the TcR gamma delta(+) population is polyclonal, as evidenced by the usage of multiple gamma and delta variable chain segm ents, Furthermore, a substantial proportion of the cells appears to be activated and these activated cells express surface activation marker s, The results clearly demonstrate that TcR gamma delta(+) cells proli ferate independently in response to a broad spectrum of challenges, Mo reover, since the expansion of the lymphoid tissues and the TcR gamma delta(+) cell population is excessive relative to that seen in wild-ty pe animals, one role of TcR alpha beta(+) cells is directly or indirec tly to limit the responses of the other lymphoid components.