IL-23/IL-17 axis in the pathogenesis and treatment of systemic lupus erythematosus and rheumatoid arthritis
- Author:
Farah Izati Aziz
1
Author Information
1. Department of Immunology, School of Medical Sciences, Universiti Sains Malaysia, 16150 Kubang Kerian, Kelantan, Malaysia
- Collective Name:Wong Kah Keng; Che Maraina Che Hussin
- Publication Type:Review
- Keywords:
IL-23;
IL-17;
Systemic lupus erythematosus;
Rheumatoid arthritis;
Therapeutic antibodies
- From:The Malaysian Journal of Pathology
2020;42(3):333-347
- CountryMalaysia
- Language:English
-
Abstract:
Interleukin-23 (IL-23) and IL-17 are the gatekeepers of CD4+
T helper 17 (Th17) cells where IL-23
is required for the development and expansion of Th17 cells that subsequently produce IL-17 to
promote inflammation. Owing to such pro-inflammatory properties, the IL-23/IL-17 axis has emerged
as an important mechanism in the pathogenesis of autoimmune diseases including systemic lupus
erythematosus (SLE) and rheumatoid arthritis (RA). In recent years, therapeutic antibodies targeting
IL-23 (e.g. ustekinumab, tildrakizumab, guselkumab) or IL-17 (e.g. brodalumab, secukinumab,
ixekizumab) have been approved for the treatment of various autoimmune diseases. In this review,
we describe the pathogenic mechanisms of IL-23/IL-17 axis in SLE and RA, as well as summarising
the findings from phase II and III clinical trials of anti-IL-23/IL-17 therapeutic antibodies in SLE and
RA patients. In particular, phase II study has demonstrated that the anti-IL-23 antibody (ustekinumab)
confers enhanced treatment outcomes in SLE patients, while anti-IL-17 antibodies (secukinumab
and ixekizumab) have shown improved clinical benefits for RA patients in phase II/III studies. Our
review highlights the emerging importance of targeting the IL-23/IL-17 axis in SLE and RA patients
- Full text:5.2020my01080.pdf
