Jl. Viney et al., LYMPHOCYTE-PROLIFERATION IN MICE CONGENITALLY DEFICIENT IN T-CELL RECEPTOR ALPHA-BETA(+) CELLS, Proceedings of the National Academy of Sciences of the United Statesof America, 91(25), 1994, pp. 11948-11952
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.