Transcription profiling of human heumatoid arthritis or common variable immunodeficiency patients reveals defective receptor editing results in the appearance of anergic B cells in humans

ABSTRACT: B cell tolerance is established using deletion, anergy and receptor editing mediated by secondary recombination but it is unclear why autoreactive B cells choose a tolerance mechanism over another. We identified subgroups of patients with either rheumatoid arthritis or common variable immunodeficiency who presented defects in secondary recombination, which correlated with unusual CD21-/lo naïve B cells in their blood. CD21-/lo B cells were unable to induce calcium flux, get activated or proliferate in response to B cell receptor and/or CD40 triggering, suggesting that these B cells are anergic. Moreover, CD21-/lo B cells are often autoreactive and may express anti-nuclear antibodies. Thus, anergy can be a default tolerance mechanism mainly induced when receptor editing fails to silence dev

ORGANISM(S): Homo sapiens

SUBMITTER: Isabelle Isnardi 

PROVIDER: E-GEOD-13917 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress