IL-23/IL-17 axis in the pathogenesis and treatment of systemic lupus erythematosus and rheumatoid arthritis.
Malays J Pathol
; 42(3): 333-347, 2020 Dec.
Article
en En
| MEDLINE
| ID: mdl-33361714
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.
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Banco de datos:
MEDLINE
Asunto principal:
Artritis Reumatoide
/
Interleucina-17
/
Interleucina-23
/
Lupus Eritematoso Sistémico
Tipo de estudio:
Etiology_studies
Límite:
Humans
Idioma:
En
Revista:
Malays J Pathol
Año:
2020
Tipo del documento:
Article
País de afiliación:
Malasia