{'fraction_non_alphanumeric': 0.026217228464419477, 'fraction_numerical': 0.0028089887640449437, 'mean_word_length': 5.1085714285714285, 'pattern_counts': {'":': 0, '<': 0, '<?xml version=': 0, '>': 0, 'https://': 0, 'lorem ipsum': 0, 'www.': 0, 'xml': 0}, 'pii_count': 0, 'substrings_counts': 0, 'word_list_counts': {'cursed_substrings.json': 0, 'profanity_word_list.json': 0, 'sexual_word_list.json': 0, 'zh_pornsignals.json': 0}}
Repertoires of antigen receptors in Tdt congenitally deficient mice.

Tdt deficient mice show lack of N region in V(D)J junctions of immunoglobulin and T cell receptor genes and revealed that "immature recombinase" in fetal stage would boil down to no more than a lack of Tdt. Although particular junctions which are thought to be created by homology-mediated joining are frequently observed, one fourth of junctions lacked even one bp of overlap, indicating the existence of a V(D)J joining pathway that is homology independent. Lymphocyte repertoire which express VH81X gene without N region is negatively selected, which shows that the repertoire of Tdt deficient mice is not a truly fetal repertoire. Positive selection of thymocytes is more efficient in Tdt deficient mice. Furthermore Tdt-/- mice produce significant amounts of anti-dsDNA antibodies as Tdt+/+ mice, indicating that increased diversity of the third complementarity-determining region (CDR3) by Tdt is not essential for the expansion of precursor B cells programmed to produce anti-DNA antibodies.