ArticleJournal of nephrology2014
Is there B cell involvement in a rat model of spontaneous idiopathic nephrotic syndrome treated with LF15-0195?
Article in Journal of nephrology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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3 authors at 2 institutions in 1 country.
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Abstract
backgroundThe Buffalo/Mna (Buff/Mna) rat spontaneously develops idiopathic nephrotic syndrome (INS), and its nephropathy recurs after the renal transplantation of a healthy graft. Only LF15-0195 is able to cause regression of the Buff/Mna nephropathy and to induce regulatory T cells, which decrease proteinuria when transferred into proteinuric Buff/Mna rats. Based on previous research on B cells in human INS, we evaluated the involvement of B cells in our model and the impact of LF15-0195.
methodsWe studied the effect of LF15-0195 on peripheral B cells by flow cytometry and quantitative reverse transcription-polymerase chain reaction. B cells were purified from LF15-0195-treated Buff/Mna rats in remission, and transferred into proteinuric Buff/Mna rats. We treated the Buff/Mna rats with mitoxantrone and measured the depletion of B/T cells in parallel with proteinuria.
resultsLF15-0195 changed the phenotype of B cells: the number of naïve mature B cells increased significantly, while the number of switched, transitional 1, and transitional 2 B cells decreased. There were no changes in the amount of memory, activated or regulatory B cells. We observed a significant increase of immunoglobulin (Ig)M mRNA transcripts in the LF15-0195-treated Buff/Mna B cells compared to controls, but no difference in the level of IgG. This profile is consistent with a block in B cell maturation at the IgM to IgG switch. The transfer of B cells from LF15-0195-treated rats into proteinuric Buff/Mna rats did not have an effect on proteinuria. Mitoxantrone, despite causing a significant depletion of B cells, did not reduce proteinuria.
conclusionDespite LF15-0195 acting on B cells, the beneficial effects of this drug on nephrotic syndrome did not involve the induction of regulatory B cells. Moreover, the B cell depletion was not effective in reducing proteinuria, indicating that B cells are not a therapeutic target.
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