Mechanisms underlying the pathophysiology of minimal-change nephrotic syndrome (MCNS), the most frequent glomerular disease in children, remain elusive, but recent findings argue for a T cell dysfunction. Starting from a differential cDNA library from T cells of a patient under relapse and remission, we identified 16 transcripts specific for MCNS. All of these transcripts that were selectively up-regulated during the relapse phase of the disease were generated by alternative splicing of known genes. This abnormal RNA expression was associated with a down-regulation of serin-rich protein 75 and serin-rich protein 40, two proteins involved in mRNA splicing. Taken together, these data suggest that T cell dysfunction in MCNS is associated with abnormal mRNA splicing.
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