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Kaneko, U. et al.

Kaneko, Toyabe, Hara, Uchiyama,

Increased mutations of CD72 transcript in B-lymphocytes from adolescent patients with systemic lupus erythematosus.

Recent studies have shown that B cells play a central role in the pathogenesis of systemic lupus erythematosus ( SLE). Abnormal expression of molecules engaging in B-cell receptor (BCR) signaling and resultant hyperactivity of B cells has been reported in both mouse models of lupus and patients with SLE. CD72 on B cells is unique in that it regulates BCR signaling both positively and negatively. We analyzed the expression of CD72 protein and mRNA in peripheral blood B cells from adolescent patients with SLE. The expression level of CD72 on B cells of the patients was decreased compared with that on B cells of controls. Sequence analysis of CD72 mRNA showed significantly increased nucleotide mutations, including both nucleotide substitutions and deletions. Almost all (95.6%) of the CD72 transcripts from the patients had different nucleotide sequences from those of the wild type. About half (41.3%) of the mutations were point mutations located close to the sequence of the immunoreceptor tyrosine-based inhibitory motif (ITIM), which negatively regulates BCR signaling. These results indicate that increased nucleotide mutation of CD72 mRNA accounts for the decreased expression level of CD72 in B cells, and it might be related to hyperactivity of B cells in patients with SLE.[1]

References

Increased mutations of CD72 transcript in B-lymphocytes from adolescent patients with systemic lupus erythematosus. Kaneko, U., Toyabe, S., Hara, M., Uchiyama, M. Pediatric allergy and immunology : official publication of the European Society of Pediatric Allergy and Immunology (2006) [Pubmed]

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