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*
Laboratory of Immune Regulations and Development, Department of Developmental Biology, and
Flow Cytometry Unit, J. Monod Institute, Centre National de la Recherche Scientifique and Universities Paris 6 and 7, Paris, France;
Sandoz Pharma, Basel, Switzerland; and
§
Division of Basic Sciences, National Jewish Center for Immunology and Respiratory Medicine, Denver, CO 80206
Although genetically different from its mother, a mammalian fetus
bearing paternal alloantigens is normally not rejected. To investigate
one of the many possible mechanisms involved in this important biologic
phenomenon, we analyzed the consequences of fetal alloantigen
recognition on maternal B lymphocytes. We used transgenic mice
expressing a unique B cell receptor with a relatively high affinity for
the MHC class I molecule H-2Kk on most B lymphocytes. We
provide the first evidence for an alloantigen-specific B cell deletion
in the spleens and bone marrow of transgenic mothers bearing
H-2Kk-positive fetuses. This highly reproducible deletion
affects 
80% of Id-bearing B cells, starts at midpregnancy, and is
only observed until term. Such a specific maternal B cell deletion
could contribute to the success of the fetal
allograft.
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