S. Santulli-marotto et al., Anti-Sm B cell differentiation in Ig transgenic MRL/Mp-1pr/1pr mice: Altered differentiation and an accelerated response, J IMMUNOL, 166(8), 2001, pp. 5292-5299
To determine the regulation of B cells specific for the ribonucleoprotein S
m, a target of the immune system in human and mouse lupus, we have generate
d mice carrying an anti-Sm H chain transgene (2-12H). Anti-Sm B cells in no
nautoimmune 2-12H-transgenic (Tg) mice are functional, but, in the absence
of immunization, circulating anti-Sm Ab levels are not different from those
of non-Tg mice. In this report, we compare the regulation of anti-Sm B cel
ls in nonautoimmune and autoimmune MRL/Mp-lpr/lpr (MRL/lpr) and bcl-2-22-Tg
mice. Activation markers are elevated on splenic and peritoneal anti-Sm B
cells of both nonautoimmune and autoimmune genetic backgrounds indicating A
g encounter. Although tolerance to Sin is maintained in 2-12H/bcl-2-22-Tg m
ice, it is lost in 2-12H-Tg MRL/lpr mice, as the transgene accelerates and
increases the prevalence of the anti-Sm response. The 2-12H-Tg MRL/lpr mice
have transitional anti-Sm B cells in the spleen similar to nonautoimmune m
ice. However, in contrast to nonautoimmune mice, there are few if any perit
oneal anti-Sm B-1 cells. These data suggest that a defect in B-1 differenti
ation may be a factor in the loss of tolerance to Sm and provide insight in
to the low prevalence of the anti-Sm response in lupus.