{'fraction_non_alphanumeric': 0.01879194630872483, 'fraction_numerical': 0.0, 'mean_word_length': 5.1652892561983474, '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}}
B cell receptor editing in tolerance and autoimmunity.

The random assembly of immunoglobulin (Ig) genes often creates a B cell receptor that is self-reactive, and such cells are subjected to negative selection. A primary mechanism to extinguish this self-reactivity is receptor editing, which allows continued recombination of Ig genes and replacement of the self-reactive receptor with a new innocuous receptor. Recent data now suggest that receptor editing may also promote autoimmunity in an autoimmune context. This mechanism has also been implicated in the process of B cell positive selection and maturation. Here we discuss the contribution of receptor editing in B-lymphopoiesis and its importance for B cell tolerance and autoimmunity.