Interleukin-17 and systemic lupus erythematosus: current concepts
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Nalbandian, A.
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Harvard Univ, Sch Med, Div Rheumatol, Beth Israel Deaconess Med Ctr,Dept Med, Boston, MA 02215 USAHarvard Univ, Sch Med, Div Rheumatol, Beth Israel Deaconess Med Ctr,Dept Med, Boston, MA 02215 USA
Nalbandian, A.
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Crispin, J. C.
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Harvard Univ, Sch Med, Div Rheumatol, Beth Israel Deaconess Med Ctr,Dept Med, Boston, MA 02215 USAHarvard Univ, Sch Med, Div Rheumatol, Beth Israel Deaconess Med Ctr,Dept Med, Boston, MA 02215 USA
Crispin, J. C.
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Tsokos, G. C.
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Harvard Univ, Sch Med, Div Rheumatol, Beth Israel Deaconess Med Ctr,Dept Med, Boston, MA 02215 USAHarvard Univ, Sch Med, Div Rheumatol, Beth Israel Deaconess Med Ctr,Dept Med, Boston, MA 02215 USA
Tsokos, G. C.
[1
]
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[1] Harvard Univ, Sch Med, Div Rheumatol, Beth Israel Deaconess Med Ctr,Dept Med, Boston, MA 02215 USA
The emerging role of interleukin (IL)-17 as a hallmark proinflammatory cytokine of the adaptive immune system, produced primarily by a new T helper cell subset termed 'Th17', has received considerable attention. Differentiation of Th17 cells is driven by the simultaneous presence of transforming growth factor-beta and certain inflammatory cytokines (e.g. IL-6, IL-21), and recent studies have shown that inflammation instigated by IL-17-producing cells is central to the development and pathogenesis of several human autoimmune diseases and animal models of autoimmunity. In this review, we focus on the information regarding IL-17 and systemic lupus erythematosus (SLE), a chronic autoimmune disease. The work that has explored the development and behaviour of IL-17-producing cells in SLE is discussed, and different mechanisms by which IL-17 could potentially augment inflammation and autoantibody production in the context of SLE are proposed.