Previous experiments with mouse chimeras demonstrated that cellular competi
tion for antigen-specific survival signals plays a crucial role in the main
tenance of the naive B cell repertoire. Transgenic (Tg) B cell populations
in these chimeras have a shortened lifespan and poor competitive abilities
as compared to more diverse non-Tg populations in the same mice. We develop
a mathematical model to investigate the mechanism of B cell competition. T
he model allows for various B cell clones, generated in the bone marrow, to
go into the peripheral circulation, where they compete specifically for va
rious ligands providing survival signals. In the model we also find the obs
erved poor competitive abilities of the Tg repertoire. Investigating the na
ture of the competition in the model, we find that most of the competition
is "intraspecific" occurring largely within the clone of truly Tg B cells,
and within the repertoire of leaky Tg and non-Tg B cells. This is confirmed
by analysing a simplified version of the model, which only allows for intr
aspecific competition, and resembles a simple ecological model with density
-dependent death. The fact that our model accounts for the data, casts doub
t on a previous interpretation of the same data arguing that more diverse r
epertoires outcompete repertoires of lower diversity. Here, we conclude tha
t most of the data can be explained with intraspecific competition, and for
mulate an experimental prediction that allows one to distinguish between th
e previous interpretation of inter-specific competition between repertoires
, and the current interpretation of intraspecific competition. (C) 2001 Aca
demic Press.