Freedom isn’t always free: immunoglobulin free light chains promote renal fibrosis
Erin B. Taylor1 and Michael J. Ryan1,2
1Department of Physiology and Biophysics, University of Mississippi Medical Center, Jackson, Mississippi, USA.
2G.V. (Sonny) Montgomery Veterans Affairs Medical Center, Jackson, Mississippi, USA.
Address correspondence to: Michael J. Ryan, Department of Physiology and Biophysics, University of Mississippi Medical Center, 2500 North State Street, Jackson, Mississippi 39216-4505. Email: mjryan@umc.edu.
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1Department of Physiology and Biophysics, University of Mississippi Medical Center, Jackson, Mississippi, USA.
2G.V. (Sonny) Montgomery Veterans Affairs Medical Center, Jackson, Mississippi, USA.
Address correspondence to: Michael J. Ryan, Department of Physiology and Biophysics, University of Mississippi Medical Center, 2500 North State Street, Jackson, Mississippi 39216-4505. Email: mjryan@umc.edu.
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Ryan, M.
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First published June 17, 2019 - More info
J Clin Invest. 2019;129(7):2660–2662. https://doi.org/10.1172/JCI129704.
© 2019 American Society for Clinical Investigation
Multiple myeloma (MM) is a relatively common hematologic malignancy, and up to half of patients with MM present with renal dysfunction at the time of diagnosis. MM-associated renal injury has been linked to an excess level of monoclonal immunoglobulin free light chains (FLCs) in the circulation; however, it is not clear how these FLCs drive renal pathology. In this issue of the JCI, Ying et al. unravel a novel mechanism by which FLCs mediate renal injury in MM by inducing fibrotic and inflammatory pathways in the kidney. Specifically, FLC-mediated production of H2O2 was shown to activate JAK2/STAT1 signaling, increase production of IL-1β via induction of capsase-1, and promote activation of TGF-β via αvβ6 integrin. Moreover, the authors identified a tryptophan residue within a specific monoclonal FLC that was required for optimal H2O2 production and downstream signaling. A better understanding of the drivers of MM-associated renal injury has potential for the identification of promising therapeutic targets.
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ISSN: 0021-9738 (print), 1558-8238 (online)