We will see if ABCs have encountered antigen and undergone somatic hypermutation and class switching. Diversity in the repertoire and the mutation frequency will be examined in old mice. This may determine if the old cells are exhausted from chronic antigen exposure. We will see if DNA repair affects the production of ABCs by using mice deficient for repair enzymes. We will also measure the frequency of chromosome translocations in these cells, to study the mechanism of how aging produces cancer.
|Vallabhaneni, Haritha; Zhou, Fang; Maul, Robert W et al. (2015) Defective repair of uracil causes telomere defects in mouse hematopoietic cells. J Biol Chem 290:5502-11|