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Institute of Experimental Immunology, Department of Pathology, University of Zürich, Zürich, Switzerland
B cell tolerance is maintained by active deletion and functional
anergy of self-reactive B cells depending on the time, amount, and site
of the self-antigen expression. To study B cell tolerance toward a
transplacentally transmitted viral Ag, we crossed transgenic mice
expressing the µ heavy and the 
light chain of the lymphocytic
choriomeningitis virus (LCMV)-neutralizing mAb KL25 (HL25-transgenic
mice) with persistently infected LCMV carrier mice. Although
HL25-transgenic LCMV carrier mice exhibited the same high virus titers
as nontransgenic LCMV carrier mice, no evidence for B cell tolerance
was found. In contrast, enhanced LCMV-neutralizing Ab titers were
measured that, however, did not clear the virus. Instead, LCMV isolates
from different tissues turned out to be neutralization resistant Ab
escape variants expressing different substitutions of amino acid
Asn119 of the LCMV-glycoprotein 1 that displays the
neutralizing B cell epitope. Virus variants with the same mutations
were also selected in vitro in the presence of the transgenic mAb KL25
confirming that substitutions of Asn119 have been selected
by LCMV-neutralizing Abs. Thus, despite abundant expression of viral
neo-self-antigen in HL25-transgenic LCMV carrier mice, transgenic B
cells expressing LCMV-neutralizing Abs were rather stimulated than
tolerized and neutralization resistant Ab escape variants were selected
in vivo.
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