Corrigendum

In 1, the author would like to change the second paragraph of the section “IL‐17, the IL‐17 receptor and signalling pathways” (page 230).

This article originally stated:

“IL‐17 binding to its receptor initiates several discrete signaling pathways, all of which are important in the pathogenesis of joint inflammation. For example, IL‐17‐induced expression of IL‐23 p19 in RA FLS is dependent on the phosphatidylinositol 3 (PI3)‐kinase/AKT (protein kinase B), natural killer (NK)‐kB, and p38 mitogen activated protein kinase (MAPK) pathways [81]. In contrast, IL‐17‐induced secretion of IL‐6 and IL‐8 from FLS is dependent on NK‐kB and PI3‐kinase/AKT, but independent of p38 MAPK signaling [23]. Thus IL‐17 utilizes multiple signalling pathways to induce various proinflammatory cytokines important in the pathogenesis of RA.”

The corrected paragraph is as follows.

“IL‐17 binding to its receptor initiates several discrete signaling pathways, all of which are important in the pathogenesis of joint inflammation. For example, IL‐17‐induced expression of IL‐23 p19 in RA FLS is dependent on the phosphatidylinositol 3 (PI3)‐kinase/AKT (protein kinase B), nuclear factor kB (NF‐kB), and p38 mitogen activated protein kinase (MAPK) pathways [81]. In contrast, IL‐17‐induced secretion of IL‐6 and IL‐8 from FLS is dependent on NK‐kB and PI3‐kinase/AKT, but independent of p38 MAPK signaling [23]. Thus IL‐17 utilizes multiple signalling pathways to induce various proinflammatory cytokines important in the pathogenesis of RA.”