Ask about this productRelated genes to: IL17F protein
- Gene:
- IL17F NIH gene
- Name:
- interleukin 17F
- Previous symbol:
- -
- Synonyms:
- IL-17F, ML-1, ML1
- Chromosome:
- 6p12.2
- Locus Type:
- gene with protein product
- Date approved:
- 2002-03-18
- Date modifiied:
- 2019-04-23
Related products to: IL17F protein
Related articles to: IL17F protein
- Psoriasis is a chronic, immune-mediated inflammatory disorder with systemic implications beyond its cutaneous manifestations. Its pathogenesis involves a complex interplay between genetic predisposition, environmental triggers, and immune dysregulation. The sustained crosstalk between dendritic cells (DCs) and T cells, which orchestrates the initiation and perpetuation of psoriatic inflammation. Plasmacytoid DCs, activated by nucleic acid-LL37 complexes, produce interferon-α that promotes myeloid DC maturation. These DCs secrete IL-12, IL-23, and TNF-α, driving differentiation of naïve T cells into Th1, Th17, and Th22 subsets. Effector T cells subsequently release cytokines such as IFN-γ, IL-17, and IL-22, which promote keratinocyte hyperproliferation, impaired differentiation, neutrophil recruitment, and angiogenesis. This DC-T cell axis forms a self-amplifying inflammatory loop that underpins disease chronicity. Conventional systemic agents, including methotrexate, cyclosporine, and retinoids, have demonstrated efficacy but are limited by nonspecific immunosuppression and significant toxicities. Advances in immunology have identified the IL-23/Th17 pathway as a pivotal therapeutic target, enabling the development of biologics and small-molecule inhibitors. Monoclonal antibodies targeting TNF-α, IL-12/23, IL-17, and IL-23 have revolutionized management, achieving high rates of sustained clearance with improved safety profiles. Additional strategies, such as PDE4 and JAK/STAT inhibitors, offer oral alternatives with targeted immunomodulation. Novel approaches, including tolerogenic DC therapy and neuroimmune modulation, hold promise for refining treatment and addressing disease heterogeneity. Effective immunotherapeutic strategies must therefore balance skin clearance with reduction of systemic inflammation and long-term comorbidity risk. Integrating mechanistic insights into DC-T cell interactions with emerging therapies provides a framework for personalized, safer, and more durable disease control. - Source: PubMed
Publication date: 2026/04/27
Kundu SharmisthaPaul RajatChakraborty Kaustav - T helper 17 (T17) cells are thought to play an important role in the pathogenesis of many autoimmune disorders, including multiple sclerosis and its animal model, experimental autoimmune encephalomyelitis (EAE). However, recent studies have suggested that interleukin-17 (IL-17) may be dispensable for the induction of EAE. Here, we use an adoptive transfer model of EAE to demonstrate that an adaptive cellular source of IL-17 is absolutely required for the induction of EAE disease. We further show that B cells can regulate the transfer of EAE disease in this context. Transcriptional profiling of T17 cells in our model suggests that loss of IL-17A/F in T cells results in a lack of an IL-23 receptor (IL-23R)-driven signaling signature. Our data demonstrate the critical importance of an adaptive immune cellular source of IL-17A and IL-17F to mediate EAE and that IL-17 signaling is required for IL-23-mediated T17 cell pathogenicity. - Source: PubMed
Publication date: 2026/04/24
Ho Allen WHuang LinglinSandhu SumitiXiao ShengSgodzai MelissaUllerich EllaKrishnan Rajesh KSchnell AlexandraKuchroo Vijay K - Rheumatoid arthritis (RA) is a persistent autoimmune disease stimulated by a sophisticated system of proinflammatory cytokines such as TNF-α and IL -17. They contribute significantly to the maintenance of inflammation and mediation of joint damage. The current study aimed to examine the relationship between serum concentrations of TNF-α, IL-17 A, and IL-17 F and disease activity in Yemeni RA patients. A case-control study was carried out on 101 RA patients and 80 healthy controls (HCs) matched for age and sex. The serum concentration of TNF-α, IL-17 A, and IL-17 F was determined through an enzyme-linked immunosorbent assay (ELISA). Other hematological, inflammatory parameters and serological tests were also assessed. TNF-α, IL-17 A and IL-17 F serum levels were significantly elevated in RA patients than in HCs (P < 0.001) and had a positive correlation with disease activity in RA groups (P < 0.001). Furthermore, a significant positive correlation between levels of TNF-α, IL-17 A, and IL-17 F and the DAS28. The ROC analysis revealed that all the three cytokines TNF-α, IL-17 A, and IL-17 F were effective in distinguishing between RA patients and HCs, with TNF-α having the highest diagnostic accuracy. To define moderate to high disease activity, IL-17 A demonstrated the best individual quality, whereas TNF-α and IL-17 F demonstrated moderate quality. Interaction of the cytokines improved the diagnostic value as both TNF-α and IL-17 A combination and triple combination of TNF-α, IL-17 A and IL17F which supports the benefits of multiplex cytokine testing in RA activity testing as well as discrimination of moderate to high activity RA. - Source: PubMed
Publication date: 2026/04/13
Saleh Amr AAl-Madhaji Anwar KAl-Shamahy Hassan AAl-Haimi Raja MSaeed Marwan K - To determine whether rapamycin affects HLA-B27-mediated gut inflammation in experimental spondyloarthritis (SpA). - Source: PubMed
Publication date: 2026/03/20
Van Doorn JinnyBrooks Stephen RLiCausi FrancescaZhou KellyBetrapally Naga SGubitz-Hess EvaCougnoux AntonyDell'Orso StefaniaIslam ShamimaColbert Robert ANavid Fatemeh - T helper 17 (Th17)-mediated skin diseases, such as psoriasis and hidradenitis suppurativa, are driven by a dysregulated cytokine network where the specific contribution of Interleukin (IL)-17F has historically been underestimated due to its lower intrinsic potency compared to IL-17 A. To elucidate the role of IL-17F in the dermal compartment, we performed bulk RNA sequencing on primary human dermal fibroblasts stimulated with recombinant IL-17 A or IL-17F, either alone or in combination with Tumor Necrosis Factor (TNF). While single stimulation confirmed the superior potency of IL-17 A, the addition of TNF completely abolished this hierarchy. Transcriptional profiling demonstrated that TNF synergizes potently with IL-17F, amplifying its inflammatory output to levels almost indistinguishable from the IL-17 A and TNF combination. This synergistic interplay drove a robust upregulation of pathogenic mediators, including neutrophil-attracting chemokines (CXCL1, CXCL8) and tissue-destructive enzymes (MMP1). These findings challenge the paradigm of IL-17F as a redundant homolog, demonstrating that within a TNF-rich pro-inflammatory environment, IL-17F overcomes its limited basal potency to mirror the inflammatory drive of IL-17 A functionally. This mechanism provides a biological rationale for the superior clinical efficacy observed with dual IL-17 A/F inhibition in chronic inflammatory skin diseases. - Source: PubMed
Publication date: 2026/04/02
Svraka LejlaAbdallah Hakim BenBertelsen TrineVestergaard ChristianJohansen Claus