Emerging Therapies in Antineutrophil Cytoplasm Antibody-Associated Vasculitis

Shunsuke Furuta; David Jayne

Disclosures

Curr Opin Rheumatol. 2014;26(1):1-6. 

In This Article

Anticytokine Therapies

Inflammatory cytokines are important components in the disease development of AAV. Among these, TNF-α is associated with disease activity in GPA and TNF-α blockade has abrogated experimental renal vasculitis.[32] Although small studies in patients with refractory disease showed promising results,[33,34] a randomized, placebo-controlled trial evaluating the efficacy of etanercept, one of the TNF-α inhibitors, in the achievement of sustained remission in GPA patients failed to show efficacy.[35] A glucocorticoid sparing role of TNF-α inhibitors in remission induction was suggested in pilot studies[36,37] of infliximab and adalimumab but their further development has not been pursued. Consequently, TNF-α inhibitors are not currently recommended in AAV therapy.

Interleukin (IL)-6 is another representative inflammatory cytokine. It was demonstrated that ANCA induced the production of IL-6 by endothelial cells in vitro,[38] and a case report suggested that tocilizumab, anti-IL-6 receptor antibody, was effective for MPA.[39]

Recently, Th17 cells have been considered to play an important role in the disease development of AAV and in early granuloma formation in GPA.[25] IL-23 is a cytokine essential for the proliferation of Th17 cells. Ustekinumab is an anti-IL-12/23p40 monoclonal antibody, and might be effective for AAV as well as other autoimmune disease related to Th17 cells such as psoriasis.

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