ArticleJournal of immunology (Baltimore, Md. : 1950)2019
Combined Blockade of TNF-α and IL-17A Alleviates Progression of Collagen-Induced Arthritis without Causing Serious Infections in Mice.
Article in Journal of immunology (Baltimore, Md. : 1950), 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
19 citing papers in PubMed, 27 citations in OpenAlex.
- The RNA binding protein Arid5a is an activator of TNF signaling in rheumatoid arthritis.JCI insight · 2026Article
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- Apoptotic cell death in disease-Current understanding of the NCCD 2023.Cell death and differentiation · 2023Review
- Dual targeted therapy in patients with psoriatic arthritis and spondyloarthritis: a real-world multicenter experience from Spain.Frontiers in immunology · 2023Article
- The forgotten key players in rheumatoid arthritis: IL-8 and IL-17 - Unmet needs and therapeutic perspectives.Frontiers in medicine · 2023Review
- Article
- Evaluating the Role of the Interleukin-23/17 Axis in Critically Ill COVID-19 Patients.Journal of personalized medicine · 2021Article
- The mScience immunology · 2021Article
- TNFα Blockade Inhibits Both Initial and Continued Control of PulmonaryFrontiers in cellular and infection microbiology · 2021Article
- Insights Into Host Cell Cytokines inFrontiers in immunology · 2021Review
- Autoimmunity in 2019.Clinical reviews in allergy & immunology · 2020Review
- The pathogenic importance of CCL21 and CCR7 in rheumatoid arthritis.Cytokine & growth factor reviews · 2020Review
- An IL-17F.S65L Knock-In Mouse Reveals Similarities and Differences in IL-17F Function in Oral Candidiasis: A New Tool to Understand IL-17F.Journal of immunology (Baltimore, Md. : 1950) · 2020Article
- Oral epithelial IL-22/STAT3 signaling licenses IL-17-mediated immunity to oral mucosal candidiasis.Science immunology · 2020Article
- [Role of tumor necrosis factor-α inNan fang yi ke da xue xue bao = Journal of Southern Medical University · 2020Article
- Regulation of host-microbe interactions at oral mucosal barriers by type 17 immunity.Science immunology · 2020Review
- The Neutrophil: Constant Defender and First Responder.Frontiers in immunology · 2020Review
- Interleukin-17A Interweaves the Skeletal and Immune Systems.Frontiers in immunology · 2020Review
- Article
Corrections and comments
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Authors and funding
12 authors at 2 institutions in 1 country.
Funding
Abstract
The cytokines TNF-α and IL-17A are elevated in a variety of autoimmune diseases, including rheumatoid arthritis. Both cytokines are targets of several biologic drugs used in the clinic, but unfortunately many patients are refractory to these therapies. IL-17A and TNF-α are known to mediate signaling synergistically to drive expression of inflammatory genes. Hence, combined blockade of TNF-α and IL-17A represents an attractive treatment strategy in autoimmune settings where monotherapy is not fully effective. However, a major concern with this approach is the potential predisposition to opportunistic infections that might outweigh any clinical benefits. Accordingly, we examined the impact of individual versus combined neutralization of TNF-α and IL-17A in a mouse model of rheumatoid arthritis (collagen-induced arthritis) and the concomitant susceptibility to infections that are likely to manifest as side effects of blocking these cytokines (oral candidiasis or tuberculosis). Our findings indicate that combined neutralization of TNF-α and IL-17A was considerably more effective than monotherapy in improving collagen-induced arthritis disease even when administered at a minimally efficacious dose. Encouragingly, however, dual cytokine blockade did not cooperatively impair antimicrobial host defenses, as mice given combined IL-17A and TNF-α neutralization displayed infectious profiles and humoral responses comparable to mice given high doses of individual anti-TNF-α or anti-IL-17A mAbs. These data support the idea that combined neutralization of TNF-α and IL-17A for refractory autoimmunity is likely to be associated with acceptable and manageable risks of opportunistic infections associated with these cytokines.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.