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Isolation and Th17 Differentiation of Naïve CD4 T Lymphocytes
Published on: September 26, 2013
Enhancing the treatment potential of IL-17 antagonism in lupus nephritis: finding the right partner
Yingying Gao1, Guoyuan Peng2, Xin Liu3,4
1Department of Rheumatology, Nantong First People's Hospital and Nantong Hospital of Renji Hospital Affiliated to Shanghai Jiao Tong University School of Medicine, Nantong, China.
The treatment of lupus nephritis (LN) has been benefiting from biologics targeting immune cells and cytokines. IL-17 antagonists have been investigated for their potential in LN treatment, with mixed results from case reports and randomized controlled trials. Here we provide an overview of the contributions of various immune cells and kidney resident cells to LN pathogenesis and discuss relevant biologics for LN treatment. We then explore our current understanding of IL-17 and IL-17-producing cells in LN pathogenesis and examine the status of IL-17 antagonists in LN treatment. Given the limited success in clinical studies with IL-17 antagonism alone for LN, we discuss possible rational combination biologic therapies, with a focus on the potential combination with antagonism of IL-36, a cytokine family associated with SLE disease activity. Thus, emerging evidence suggests that dual biologic therapy could enhance disease control in LN.
The treatment of lupus nephritis (LN) has been benefiting from biologics targeting immune cells and cytokines. IL-17 antagonists have been investigated for their potential in LN treatment, with mixed results from case reports and randomized controlled trials. Here we provide an overview of the contributions of various immune cells and kidney resident cells to LN pathogenesis and discuss relevant biologics for LN treatment. We then explore our current understanding of IL-17 and IL-17-producing cells in LN pathogenesis and examine the status of IL-17 antagonists in LN treatment. Given the limited success in clinical studies with IL-17 antagonism alone for LN, we discuss possible rational combination biologic therapies, with a focus on the potential combination with antagonism of IL-36, a cytokine family associated with SLE disease activity. Thus, emerging evidence suggests that dual biologic therapy could enhance disease control in LN.
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