A polymorphism in the interleukin-4 receptor affects the ability of interleukin-4 to regulate Th17 cells: a possible immunoregulatory mechanism for genetic control of the severity of rheumatoid arthritis |
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| Authors: | Susan K Wallis Laura A Cooney Judith L Endres Min Jie Lee Jennifer Ryu Emily C Somers David A Fox |
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| Institution: | (1) Division of Rheumatology and Rheumatic Diseases Research Core Center, Department of Internal Medicine, University of Michigan, 1500 East Medical Center Drive, Ann Arbor, MI 48109, USA |
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| Abstract: | Introduction Rheumatoid arthritis (RA) is now suspected to be driven by pathogenic Th17 cells that secrete interleukin (IL)-17 and can
be regulated by IL-4. A single-nucleotide polymorphism (SNP), I50V, in the coding region of the human IL-4 receptor (IL-4R)
is associated with rapid development of erosive disease in RA. The present study was undertaken to determine whether this
SNP renders the IL-4R less able to transduce signals that regulate IL-17 production. |
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