IL-23-IL-17 immune axis: Discovery, Mechanistic Understanding, and Clinical Testing

By S. Gaffen, Renu Jain, A. Garg, D. Cua. 2014

1,483 citations recorded by the source corpus.

Following the discovery of T helper 17 (TH17) cells, the past decade has witnessed a major revision of the TH subset paradigm and substantial progress has been made in deciphering the molecular mechanisms of T cell lineage commitment and function. In this Review, we focus on the recent advances that have been made regarding the transcriptional control of TH17 cell plasticity and stability, as well as the effector functions of TH17 cells, and we highlight the mechanisms of IL-17 signalling in mesenchymal and barrier epithelial tissues. We also discuss the emerging clinical data showing that IL-17-specific and IL-23-specific antibody treatments are remarkably effective for treating many immune-mediated inflammatory diseases.

Subfields: Immunology

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In Immunology

1. S. Gaffen
2. D. Cua
3. M. McGeachy
4. A. Garg
5. Nilesh Amatya
6. C. Rosales
7. Erika L. Pearce
8. R. Flavell

Citations in the corpus

• Structural activation of pro-inflammatory human cytokine IL-23 by cognate IL-23 receptor enables recruitment of the shared receptor IL-12Rβ1 (2017, background): “…( IL-12 , IL-23, IL-27, IL-35 IL-35) are predominantly produced by It is precisely the potency by which IL-23 can drive production of interleukin-17 (IL-17) by Th17 cells and IL-17-producing γδ T ( γδ T17) cells, that has propelled IL-23 to a major therapeutic target (Gaffen et al., 2014).”
• The IL-17 family of cytokines in health and disease (2019, background): “Additionally, IL-17 induces IL-6 and G-CSF, cytokines that promote myeloid-driven innate inflammation (Gaffen et al., 2014).”
• IL-17 Signaling: The Yin and the Yang (2017, background): “Myeloid cells have also been reported to make IL-17, although not in large amounts, and in many cases the validity of this has been called into question [7].”
• Neutrophil: A Cell with Many Roles in Inflammation or Several Cell Types? (2018, background): “In this mechanism, macrophages and also dendritic cells phagocytose apoptotic neutrophils (Gordy et al., 2011; Jiao et al., 2014) leading to a reduction on IL-23 (Stark et al., 2005), which in turn controls expression of IL-17 by T lymphocytes (Gaffen et al., 2014).”
• Unraveling the Complex Interplay Between T Cell Metabolism and Function (2018, background): “immunity, but pathogenic Th17 cells, which make IFN-γ in addition to IL-17, are the cause of a number of inflammatory diseases (120).”
• Update on the Pathomechanism, Diagnosis, and Treatment Options for Rheumatoid Arthritis (2020, background): “Th17 cells, induced by the cytokines IL-6, IL-1β, IL-21, TGF-β, and IL-23 present in synovial joints [48,49], were shown to recruit neutrophils, activate B cells, and promote osteoclastogenesis [50,51].”