The relationship between somatic hypermutation and affinity maturation
in the mouse is delineated. Recent work on the anatomical and cellula
r site of this process is surveyed. The molecular characteristics of s
omatic hypermutation are described in terms of the region mutated and
the distinctive patterns of nucleotide changes that are observed. The
results of experiments utilizing transgenic mice to find out the minim
um cis-acting sequences required to recruit hypermutation are summariz
ed. The hypothesis that V gene sequences have evolved in order to targ
et mutation to certain sites but not others is discussed. The use that
different species make of somatic hypermutation to generate either th
e primary or secondary B cell repertoire is considered. Possible molec
ular mechanisms for the hypermutation process and future goals of rese
arch are outlined.