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The molecular mechanisms that lead to autoantibody production and autoimmune disease remain poorly defined. Based on a clinical observation in a patient with lupus erythematosus and autoimmune hepatitis we here provide the first evidence that (i) a particular cytogenetic aberration (deletion (13)(q14)) could be detected in a proportion of plasma cells and that (ii) the surface marker CD56 could be used to enrich for plasma cells with this cytogenetic aberration.
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