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Bibliometric analysis on the structure and function of IL17

Abstract

Background

Interleukin17 (IL17) is an important cytokine in host defense at mucosal surfaces and also mediates many autoimmune diseases, including rheumatoid arthritis (RA). In recent years, many types of research relevant to the structure and function of IL17 have been identified. However, there is no bibliometric analysis in this research field. This study aims to explore the history, research hotspots, and emerging trends of IL17 from the perspective of the structure and function dynamics.

Methods

Articles relevant to IL17 in the last two decades were retrieved through the Web of Science Core Collection (WoSCC) database. The bibliometric analysis was performed by VOSview.

Results

A total of 882 papers in this research were analyzed from 65 countries, and the rate of published articles has increased from 2008 annually, with the USA, China, and Germany leading the research effort. Frontiers in Immunology has significantly impacted research in this field and the University of Pittsburgh was the leading institution. Gaffen, Sarah L. from the University of Pittsburgh was the most productive researcher in this field and Papp Ka from the Probity Medical Research Incorporate of Canada is the most co-cited author. The analysis of keywords showed that inflammation, expression, Th17 cells, and cytokines were the main hotspots and frontier directions of IL17. The trend of clinical application in the future is the development of new therapy drugs based on the structure of IL17 or IL17 signaling pathway molecular.

Conclusions

Our research summarized the developments and research trends of IL17 and would help researchers understand the research status of IL17 and provide a reference for future researchers as soon as possible.

Background

Interleukin-17 (IL17) discovered in 1999 from the joints of rheumatoid arthritis (RA) patients [1] is a highly versatile proinflammatory and T helper 17 (Th17) cytokines and is involved in host defense, tissue repair, cancer progression, and many autoimmune diseases [2]. In autoimmune-RA diseases, IL17 is involved in promoting the activation of fibroblast-like synoviocytes (FLS), osteoclastogenesis, and recruitment and activation of neutrophils, macrophages, and B cells [3].

IL17 is a glycoprotein containing 155 amino acids and contains 6 family members (IL17A-F) [4]. As IL-17RA is a receptor shared by the ligands of the IL-17 family, the receptor correspondingly has 5 family members (IL17RA-RE). IL-17A and IL-17F exist as homodimers or heterodimers, and various forms of cytokines induce downstream signals through specific dimeric IL-17RA and IL-17RC receptor complexes. IL17A was first discovered from a rodent T cell by Rouvier et al. in 1993 and contained a highly conserved cysteine-knot fold structure in the C-terminal [5]. Unlike IL17A detected in activated CD4 T cells, IL17B mainly expresses in neutrophils, chondrocytes, and native, memory, and germinal center B cells and was also detected in rheumatoid synovial tissues from rheumatic arthritis patients [6,7,8,9,10]. IL17B consists of 180 amino acids and assembles a non-covalent dimer glycoprotein [11]. IL17C was reported to bind to IL17RE and activate the NF-κB pathway. However, the ligands for IL17RD have yet to be identified. Meanwhile, the heterodimer consisting of IL17RA and IL17RB serves as a receptor for IL17E. Variants of IL17 and their potential role are summarized and shown in Table 1. IL17R contains a conserved extracellular fibronectin III-like domain and SEFIR (similar expression to fibroblast growth factor genes and IL17R) domain which recruits the cytoplasmic adaptor protein Act1 via SEFIR-SEFIR interaction [12].

Table 1 Different variants of IL17 and their potential role

Recently, structure-based drug design was used to guide the optimization of a series of selective IL17 or IL17R inhibitors in preclinical development. IL17 inhibitors have been studied to therapy clinical diseases such as psoriatic (PSO), psoriatic arthritis (PSA), and ankylosing spondylitis (AS) [13]. Secukinumab and ixekizumab are both antibodies of IL17A but are not effective on IL17F [14, 15]. Brodalumab targets IL17R which can neutralize IL17RA with high affinity [16]. Besides biological therapy, small molecule inhibitors targeting IL17A signaling ligand also have been developed and some studies have been vindicated that some macrocycles may more efficiently interfere with the IL17A binding with IL17RA compared to that of antibodies [17].

The bibliometric analysis focuses on the publications in a specific research field and can visually depict the distribution, research status, hotspots, and development trend to allow researchers to easily access relevant scientific information and serve as a useful reference or guide [18,19,20]. Up to now, the study of IL17 structure and function has not been analyzed by bibliometric analysis. Our study provides a comprehensive understanding of the current state and trends in the field purposing to promote the development of IL17 study in various diseases.

Methods

Data collection and statistics

The data were collected from the Web of Science Core Collection (WoSCC) database (https://www.webofscience.com/wos/woscc/basic-search). This paper set (“IL17” OR “Interleukin-17” OR “IL-17 receptor” OR “IL17R”) AND (“Structure*” OR “Structural” OR “Structure–function” OR “Structure-targeting” OR “Targeting”) as the retrieval condition, with a time interval of 1998–2023 and literature types selected as “Article” and “Review Article”. Analyses were conducted on Jun 13, 2023. Then 882 literature records were retrieved, downloaded, and saved as a plain text file in the format of “Full Record and Cited References”.

Data analysis

The data obtained from WoSCC were processed and analyzed by the bibliometric analysis software VOSviewer. The different nodes in the figure map represent items such as countries, institutions, authors, and hotspots; the size of the nodes indicates the number of these elements; and the lines between nodes show the degree of cooperation or co-cited of the project. The quantitative analysis of publications distribution was analyzed by Microsoft Office Excel 2009.

Results

Quantitative analysis of annual publications distribution

The annual research outputs from 1998 to 2023 are shown in Fig. 1A. 1998 was the first year that an IL17-related gut epithelial paper was published. The number of publications was relatively small between 2000 and 2007. Overall, annual publications about IL17 increased rapidly since 2008. Moreover, Frontiers In Immunology ranked the top in the number of published (34), followed by Plos One (22) and International Journal Of Molecular Sciences (13) as shown in Fig. 1B.

Fig. 1
figure 1

A Annual number of publications in structure and function research of IL17 from 1998 to 2023. B The top 15 fruitful journals. Numbers represent the publication’s quantity

Distribution characteristics of countries/regions and institutions

Between 1998 and 2023, 65 countries published studies related to the structure and function of IL17. The top ten countries with the highest number of publications are distributed in North America, Asia, and Europe. Among the top 10 countries (Table 2), the USA had the highest number of publications (n = 300), followed by China (n = 216), and Germany (n = 70). As shown in Fig. 2A, the network nodes of the USA, China, and Germany are located at the center of the cooperation relationship map with multiple links with the other major issuing countries. The top ten institutions are in the USA and China (Table 2 right (from the institution line)). The collaboration network between institutions was also analyzed by VOSviewer (Fig. 2B). The top 10 contributing institutions published 855 articles, accounting for 97%. And the University of Pittsburgh in Southwestern of Pennsylvania, USA, contributed the most to the body of knowledge (n = 16), followed by the University of Lyon (n = 14), Chinese Academy Sciences (n = 13), and Fudan University (n = 13).

Table 2 The Top10 countries and institutions contributing to publications in IL17
Fig. 2
figure 2

Main countries and institutions related to the structure and function research of IL17. A A visualization network of collaboration between countries in the structure and function research of IL17. B A visualization network of collaboration among institutions in the structure and function research of IL17

Analysis of top authors and co-cited authors

A collaboration between authors was shown in Fig. 3A and the top 10 authors was tabulated in Table 3 based on the authors’ published papers. Gaffen, Sarah L. and Kolls, Jay K. from the University of Pittsburgh focused on the structure and function of IL17R, and the receptors of IL17 family members bind with [21,22,23,24]. Pierre Miossec, Marije I. Koenders, and Erik Lubberts from the University of Lyon focused on the mechanism and targeting function of IL17 in various diseases [1, 25, 26].

Fig. 3
figure 3

Visualization of authors (A) and co-cited authors (B) in the structure and function research of IL17

Table 3 Top 10 authors and co-cited authors on the research of IL17

The top 10 co-cited authors are shown in Table 3 (right (from the co-cited authors line)), and 302 authors (minimum co-citation number of an author equal to 20) were filtered to draw the co-citation network (Fig. 3B). Analysis showed that Papp Ka, Mease Pj, and Gaffen Sl et al. have an important influence in the structure and function research of IL17. Papp Ka from Probity Medical Research Incorporated of Canada is engaged in the targeting therapy of IL17 in various diseases [27, 28]. Mease Pj from the University of Washington (the USA) is studying the drug and mechanism for inhibiting IL17 in arthritis [29, 30]. Gaffen Sl from the University of Pittsburgh (the USA) is to explain the structure and signaling of IL17 [2, 31, 32].

Analysis of hotspots and frontiers

Hotspots is a key methodology in bibliometric analysis to point topic in a specific research area during a certain period of time. Keyword burst patterns were detected to reveal active contents in IL17 through the co-occurrence analysis of keywords. Following a previous study [33], keywords with similar meanings were merged, then for keyword analysis. The network visualization of keywords is shown in Fig. 4. The size of nodes mirrors the occurrence frequency of keywords and the distance between two nodes reflects the strength of their association. The top 20 high-frequency keywords are shown in Table 4.

Fig. 4
figure 4

Analysis of the research hotspots of IL17, A network visualization of author keywords and B overlay visualization of author keywords

Table 4 Top 20 keywords on the research of IL17

Keywords with a closer distance were classified into the same cluster, which roughly reflects the main topics in the research area [34]. Among these keywords, “Inflammation”, “Expression”, “Th17 cells”, and “Cytokines” appeared more than 200 times, representing the main research direction of IL17. The keywords “Rheumatoid arthritis”, “Trial”, and “Psoriatic spondylitis” are related to the role of IL17 in pathogenesis. As shown in Fig. 4A, the keywords in red clusters consist of inflammation, expression, Th17 cells, and cytokines, in blue clusters consist of rheumatoid arthritis, and in green clusters consist of trial and psoriatic spondylitis. The overlay visualization of author keywords is presented in Fig. 4B. The keywords colored in yellow represent those that have appeared recently. Keywords, such as “secukinumab”, “mechanism”, “plaque psoriasis”, “psoriatic arthritis”, and “ankylosing spondylitis” represent the main research direction in recent years. The keyword “secukinumab” associates with developing novel targeted drugs for IL17 and the keyword “mechanism” may be related to the signaling pathway of IL17 in various diseases and the interaction structure between IL17 and IL17R. The keywords “plaque psoriasis”, “psoriatic arthritis”, and “ankylosing spondylitis” implicate some autoimmune disease hotspots of IL17.

Analysis of reference with co-citation

Reference co-citation can be used to reflect the most-cited papers [35]. The co-citation network was drawn (Fig. 5) after filtering out references with a minimum number of co-citations is 60. The top 10 references that were co-cited were listed in Table 5. The reference “Park H, 2005, nat immunol, v6, p1133, https://doi.org/10.1038/ni1261” was co-cited up to 113 times [36].

Fig. 5
figure 5

Visualization of co-cited references on the research of IL17

Table 5 Top 10 co-cited references on the research of IL17

Discussion

General information

Many high-quality studies on the structure and function of IL17 have been published. This bibliometric study analyzed the development of IL17 since it was first studied. Articles on IL17 showed a rapidly growing trend since 2008. Meanwhile, the number of articles about IL17 stationary fluctuated at 80 per year since 2018. Most of these articles were mainly published in journals Frontiers in Immunology, Plos One, and International Journal of Molecular Sciences.

Among the 65 countries contributing to the IL17 research, the USA led the way with the largest number of publications, citations, and link strength with other countries. Moreover, Gaffen, Sarah L. from the University of Pittsburgh in the USA mainly focused on the structure of IL17-IL17R and the downstream signaling pathway of IL17. China was the second most productive country where the institution—Chinese Academy Sciences having the most publications. Germany and Italy also contribute to the research of IL17. Miossec, Pierre from the University of Lyon published articles following Gaffen, Sarah L. mainly focuses on targeting therapy of IL17 in various diseases. Among the top 10 cited articles analyzed in this study, the key focus was inflammation response, expression in various diseases such as rheumatoid arthritis and psoriatic spondylitis and targeting drug of IL17 [14, 37, 38].

Research basis

In 1998, recombinant hIL17 was first cloned from a Pichia pastoris expression to study the structure and function of IL17 [39]. Following, the binding signaling pathway of IL17 and targeting therapy were revealed in autoimmune disease. The common pathway is the IL17 recruited to their receptors (IL17R) through specificity heterotypic interactions between the SEFIR domain (CC′ loop motif) of Act1 and that of IL17R [40]. Secukinumab, ixekizumab, and Brodalumab which are recombinant fully human monoclonal anti-IL17A antibody enable the effects of IL17A inhibition in multiple autoimmune diseases [41,42,43]. As IL17 arises directly from Th17 cells and targeting IL17 alone is not sufficient to improve clinical endpoints, targeting the IL17 and Th17 cell lineage may be superior to blocking a single effector cytokine [44].

IL17A is associated with RA due to IL17A expression in RA synovial fluid. RA is a systemic poly-articular autoimmune pathology [45] and affects an average of 1% of the adult population worldwide [46]. The common damage in rheumatoid arthritis is joints and extra-articular organs [47]. Although the etiology of RA is not yet fully understood, researchers have studied that IL17 induces downstream cytokine production through NF-κB and PI3K/Akt-dependent pathways [48]. Targeting IL17 and Th17 pathway therapy has been experimented with in RA model [26, 49]. Currently, many nonsteroidal anti-inflammatory drugs (NSAIDs), corticosteroids (SAIDs), and analgesics have been used to decrease inflammatory and immunosuppressive effects during RA treatment [50]. Although the above agents have mitigated the RA pain [51], it is still needed to research and explore new methods to achieve the maximum therapeutic effectiveness.

Ankylosing spondylitis is a chronic inflammatory disease involving the axial spine which can manifest with various clinical signs and symptoms [52]. IL17A antagonists such as Secukinumab and ixekizumab have been explored to treat ankylosing spondylitis [53]. Recently, netakimab, a novel IL17 inhibitor in clinical trials, has established a therapeutic dose in patients with active ankylosing spondylitis [54] and Iguratimod, a novel small molecule drug, also has shown efficacy treatment [55]. Psoriatic spondylitis belongs to the family of ankylosing spondylitis, and novel nonbiological small molecules, such as Janus kinase (JAK) inhibitors, are being evaluated in clinical trials for this disease [56, 57]. Together, these findings clarify the critical role of IL17 in pathogenesis and targeted therapy research in a variety of diseases.

Future directions

Secukinumab, the first antibody against IL-17A, was approved in 2015 for the treatment of plaque psoriasis, psoriatic arthritis, and ankylosing spondylitis, followed by ixekizumab and brodalumab for clinical trials in psoriasis and other IL-17 or IL-17R inhibitors. However, multiple clinical trials of secukinumab and brodalumab in IL-17-related diseases were discontinued due to no or limited clinical effect [58,59,60]. Recently, studies found that targeting Act1-SHP2 which is the downstream signaling molecule of IL17 inhibits IL17-related diseases resistant to anti-IL17 therapy (an autonomous activation of interleukin-17 receptor signaling sustains inflammation and promotes disease progression) [61]. This may indicate that the downstream molecule of IL17 can be a target for drug discovery and various autoimmune diseases may exist an autonomous activation of receptor signaling which suggests a new therapeutic research idea.

In conclusion, this study provides insight into the research trends and developments of IL17 by bibliometrics analysis, which may guide new directions for further study.

Conclusion

Drug target IL17 has been mostly studied for the treatment of various autoimmune diseases, such as RA and PSO in recent years. We report about the history, research hotspots, and emerging trends of IL17 from the perspective of the structure and function dynamics in the last two decades with bibliometric methods. IL17 has been extensively studied in rheumatism, and biologic therapy targeting IL17 antibodies is expected to be a new approach to the treatment of rheumatoid arthritis. Our research summarized the developments and research trends of IL17 and would help researchers understand the research status of IL17 and provide a reference for future researchers as soon as possible.

Availability of data and materials

We approve the availability of our data upon request.

Abbreviations

APCs:

Antigen-presenting cells

AS:

Ankylosing spondylitis

DC:

Dendritic cells

FLS:

Fibroblast-like synoviocytes

IL17:

Interleukin 17

JAK:

Janus kinase

NK:

Natural killer

NSAIDs:

Nonsteroidal anti-inflammatory drugs

PSA:

Psoriatic arthritis

PSO:

Psoriatic

RA:

Rheumatoid arthritis

SAIDs:

Corticosteroids

SEFIR:

Similar expression to fibroblast growth factor genes and IL17R

Th17:

T helper 17

WoSCC:

Web of Science Core Collection

References

  1. Beringer A, Noack M, Miossec P (2016) IL-17 in chronic inflammation: from discovery to targeting. Trends Mol Med 22(3):230–241

    Article  CAS  PubMed  Google Scholar 

  2. McGeachy MJ, Cua DJ, Gaffen SL (2019) The IL-17 family of cytokines in health and disease. Immunity 50(4):892–906

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  3. Lubberts E (2015) The IL-23-IL-17 axis in inflammatory arthritis. Nat Rev Rheumatol 11(10):562

    Article  PubMed  Google Scholar 

  4. Gu C, Wu L, Li X (2013) IL-17 family: cytokines, receptors and signaling. Cytokine 64(2):477–485

    Article  CAS  PubMed  Google Scholar 

  5. Weaver CT, Hatton RD, Mangan PR et al (2007) IL-17 family cytokines and the expanding diversity of effector T cell lineages. Annu Rev Immunol 25:821–852

    Article  CAS  PubMed  Google Scholar 

  6. Li H, Chen J, Huang A et al (2000) Cloning and characterization of IL-17B and IL-17C, two new members of the IL-17 cytokine family. Proc Natl Acad Sci U S A 97(2):773–778

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  7. Kouri VP, Olkkonen J, Ainola M et al (2014) Neutrophils produce interleukin-17B in rheumatoid synovial tissue. Rheumatology (Oxford) 53(1):39–47

    Article  CAS  PubMed  Google Scholar 

  8. Kokubu T, Haudenschild DR, Moseley TA et al (2008) Immunolocalization of IL-17A, IL-17B, and their receptors in chondrocytes during fracture healing. J Histochem Cytochem 56(2):89–95

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  9. Moore EE, Presnell S, Garrigues U et al (2002) Expression of IL-17B in neurons and evaluation of its possible role in the chromosome 5q-linked form of Charcot-Marie-Tooth disease. Neuromuscul Disord 12(2):141–150

    Article  PubMed  Google Scholar 

  10. Ferretti E, Ponzoni M, Doglioni C et al (2016) IL-17 superfamily cytokines modulate normal germinal center B cell migration. J Leukoc Biol 100(5):913–918

    Article  CAS  PubMed  Google Scholar 

  11. Kolls JK, Linden A (2004) Interleukin-17 family members and inflammation. Immunity 21(4):467–476

    Article  CAS  PubMed  Google Scholar 

  12. Iwakura Y, Ishigame H, Saijo S et al (2011) Functional specialization of interleukin-17 family members. Immunity 34(2):149–162

    Article  CAS  PubMed  Google Scholar 

  13. Braun J, Schwarting A, Hammel L et al (2019) Medical care situation of patients with ankylosing spondylitis and psoriatic arthritis in Germany: medical care situation of patients with spondyloarthritis (SpA): ankylosing spondylitis (AS) and psoriatic arthritis (PsA) from the perspective of rheumatologists in private practice and hospitals in Germany-Results of the research project “SpA Loop-Life of Outpatients.” Z Rheumatol 78(4):372–381

    Article  CAS  PubMed  Google Scholar 

  14. Langley RG, Elewski BE, Lebwohl M et al (2014) Secukinumab in plaque psoriasis–results of two phase 3 trials. N Engl J Med 371(4):326–338

    Article  PubMed  Google Scholar 

  15. Griffiths CE, Reich K, Lebwohl M et al (2015) Comparison of ixekizumab with etanercept or placebo in moderate-to-severe psoriasis (UNCOVER-2 and UNCOVER-3): results from two phase 3 randomised trials. Lancet 386(9993):541–551

    Article  CAS  PubMed  Google Scholar 

  16. Tomalin LE, Russell CB, Garcet S et al (2020) Short-term transcriptional response to IL-17 receptor-A antagonism in the treatment of psoriasis. J Allergy Clin Immunol 145(3):922–932

    Article  CAS  PubMed  Google Scholar 

  17. Wang W, Groves MR, Domling A (2018) Artificial macrocycles as IL-17A/IL-17RA Antagonists. Medchemcomm 9(1):22–26

    Article  CAS  PubMed  Google Scholar 

  18. Peng C, Kuang L, Zhao J et al (2022) Bibliometric and visualized analysis of ocular drug delivery from 2001 to 2020. J Control Release 345:625–645

    Article  CAS  PubMed  Google Scholar 

  19. Benita F (2021) Human mobility behavior in COVID-19: a systematic literature review and bibliometric analysis. Sustain Cities Soc 70:102916

    Article  PubMed  PubMed Central  Google Scholar 

  20. Grover S, Elwood AD, Patel JM et al (2022) Altmetric and bibliometric analysis of obstetrics and gynecology research: influence of public engagement on citation potential. Am J Obstet Gynecol 227(2):300 e301-300 e344

    Article  Google Scholar 

  21. Ho AW, Gaffen SL (2010) IL-17RC: a partner in IL-17 signaling and beyond. Semin Immunopathol 32(1):33–42

    Article  CAS  PubMed  Google Scholar 

  22. Shen F, Gaffen SL (2008) Structure-function relationships in the IL-17 receptor: implications for signal transduction and therapy. Cytokine 41(2):92–104

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  23. Ramani K, Garg AV, Jawale CV et al (2016) The Kallikrein-Kinin system: a novel mediator of IL-17-driven anti-Candida immunity in the kidney. PLoS Pathog 12(11):e1005952

    Article  PubMed  PubMed Central  Google Scholar 

  24. Crowe CR, Chen K, Pociask DA et al (2009) Critical role of IL-17RA in immunopathology of influenza infection. J Immunol 183(8):5301–5310

    Article  CAS  PubMed  Google Scholar 

  25. Toh ML, Gonzales G, Koenders MI et al (2010) Role of interleukin 17 in arthritis chronicity through survival of synoviocytes via regulation of synoviolin expression. PLoS One 5(10):e13416

    Article  PubMed  PubMed Central  Google Scholar 

  26. Roeleveld DM, van Nieuwenhuijze AE, van den Berg WB et al (2013) The Th17 pathway as a therapeutic target in rheumatoid arthritis and other autoimmune and inflammatory disorders. BioDrugs 27(5):439–452

    Article  CAS  PubMed  Google Scholar 

  27. Reich K, Papp KA, Matheson RT et al (2015) Evidence that a neutrophil-keratinocyte crosstalk is an early target of IL-17A inhibition in psoriasis. Exp Dermatol 24(7):529–535

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  28. Gudjonsson J, Tsoi LC, Blauvelt A, Papp KA, Dow ER, Gemperline DC, Elmaraghy H, Krishnan V (2023) 581 Ixekizumab reduces key IL-17 and IL-23 pathway genes more rapidly than guselkumab: 4-week results from IXORA-R. J Investig Dermatol 143:S100

    Article  Google Scholar 

  29. Mease PJ (2015) Inhibition of interleukin-17, interleukin-23 and the TH17 cell pathway in the treatment of psoriatic arthritis and psoriasis. Curr Opin Rheumatol 27(2):127–133

    Article  CAS  PubMed  Google Scholar 

  30. Genovese MC, Weinblatt ME, Mease PJ et al (2018) Dual inhibition of tumour necrosis factor and interleukin-17A with ABT-122: open-label long-term extension studies in rheumatoid arthritis or psoriatic arthritis. Rheumatology (Oxford) 57(11):1972–1981

    Article  CAS  PubMed  Google Scholar 

  31. Bechara R, McGeachy MJ, Gaffen SL (2021) The metabolism-modulating activity of IL-17 signaling in health and disease. J Exp Med 218(5):e20202191

  32. Cruz JA, Childs EE, Amatya N et al (2017) Interleukin-17 signaling triggers degradation of the constitutive NF-kappaB inhibitor ABIN-1. Immunohorizons 1(7):133–141

    Article  CAS  PubMed  Google Scholar 

  33. Wu H, Zhou Y, Wang Y et al (2021) Current state and future directions of intranasal delivery route for central nervous system disorders: a scientometric and visualization analysis. Front Pharmacol 12:717192

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  34. Sun HL, Bai W, Li XH et al (2022) Schizophrenia and inflammation research: a bibliometric analysis. Front Immunol 13:907851

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  35. Li JGF, Reniers G (2020) Trevor Kletz’s scholarly legacy: a co-citation analysis. J Loss Prev Process Ind 66:104166

    Article  Google Scholar 

  36. Park H, Li Z, Yang XO et al (2005) A distinct lineage of CD4 T cells regulates tissue inflammation by producing interleukin 17. Nat Immunol 6(11):1133–1141

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  37. Langrish CL, Chen Y, Blumenschein WM et al (2005) IL-23 drives a pathogenic T cell population that induces autoimmune inflammation. J Exp Med 201(2):233–240

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  38. Fossiez F, Djossou O, Chomarat P et al (1996) T cell interleukin-17 induces stromal cells to produce proinflammatory and hematopoietic cytokines. J Exp Med 183(6):2593–2603

    Article  CAS  PubMed  Google Scholar 

  39. Murphy KP Jr, Gagne P, Pazmany C et al (1998) Expression of human interleukin-17 in Pichia pastoris: purification and characterization. Protein Expr Purif 12(2):208–214

    Article  CAS  PubMed  Google Scholar 

  40. Liu C, Swaidani S, Qian W et al (2011) A CC’ loop decoy peptide blocks the interaction between Act1 and IL-17RA to attenuate IL-17- and IL-25-induced inflammation. Sci Signal 4(197):ra72

    Article  PubMed  PubMed Central  Google Scholar 

  41. Patel DD, Lee DM, Kolbinger F et al (2013) Effect of IL-17A blockade with secukinumab in autoimmune diseases. Ann Rheum Dis 72 Suppl 2:ii116-123

    Article  PubMed  Google Scholar 

  42. Dyring-Andersen B, Skov L, Zachariae C (2015) Targeting IL-17 with ixekizumab in patients with psoriasis. Immunotherapy 7(9):957–966

    Article  CAS  PubMed  Google Scholar 

  43. Roostaeyan O, Kivelevitch D, Menter A (2017) A review article on brodalumab in the treatment of moderate-to-severe plaque psoriasis. Immunotherapy 9(12):963–978

    Article  CAS  PubMed  Google Scholar 

  44. Yang J, Sundrud MS, Skepner J et al (2014) Targeting Th17 cells in autoimmune diseases. Trends Pharmacol Sci 35(10):493–500

    Article  CAS  PubMed  Google Scholar 

  45. Singh E, Osmani RAM, Banerjee R et al (2022) Poly epsilon-Caprolactone nanoparticles for sustained intra-articular immune modulation in adjuvant-induced arthritis rodent model. Pharmaceutics 14(3):519

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  46. Isaacs JD (2010) The changing face of rheumatoid arthritis: sustained remission for all? Nat Rev Immunol 10(8):605–611

    Article  CAS  PubMed  Google Scholar 

  47. Cojocaru M, Cojocaru IM, Silosi I et al (2010) Extra-articular manifestations in rheumatoid arthritis. Maedica (Bucur) 5(4):286–291

    PubMed  Google Scholar 

  48. Hwang SY, Kim JY, Kim KW et al (2004) IL-17 induces production of IL-6 and IL-8 in rheumatoid arthritis synovial fibroblasts via NF-kappaB- and PI3-kinase/Akt-dependent pathways. Arthritis Res Ther 6(2):R120-128

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  49. Chao CC, Chen SJ, Adamopoulos IE et al (2011) Anti-IL-17A therapy protects against bone erosion in experimental models of rheumatoid arthritis. Autoimmunity 44(3):243–252

    Article  CAS  PubMed  Google Scholar 

  50. Vojdanian M, Ahmadi H, Jamshidi AR et al (2017) The anti-migraine effects of M2000 (beta-D-mannuronic acid) on a patient with rheumatoid arthritis: case report. Curr Clin Pharmacol 12(2):127–130

    Article  CAS  PubMed  Google Scholar 

  51. Mittal N, Mittal R, Sharma A et al (2012) Treatment failure with disease-modifying antirheumatic drugs in rheumatoid arthritis patients. Singapore Med J 53(8):532–536

    PubMed  Google Scholar 

  52. Wendling D, Verhoeven F, Prati C (2019) Anti-IL-17 monoclonal antibodies for the treatment of ankylosing spondylitis. Expert Opin Biol Ther 19(1):55–64

    Article  CAS  PubMed  Google Scholar 

  53. Dubash S, Bridgewood C, McGonagle D et al (2019) The advent of IL-17A blockade in ankylosing spondylitis: secukinumab, ixekizumab and beyond. Expert Rev Clin Immunol 15(2):123–134

    Article  CAS  PubMed  Google Scholar 

  54. Erdes S, Nasonov E, Kunder E et al (2020) Primary efficacy of netakimab, a novel interleukin-17 inhibitor, in the treatment of active ankylosing spondylitis in adults. Clin Exp Rheumatol 38(1):27–34

    PubMed  Google Scholar 

  55. Liu S, Cui Y, Zhang X (2021) Molecular mechanisms and clinical studies of iguratimod for the treatment of ankylosing spondylitis. Clin Rheumatol 40(1):25–32

    Article  PubMed  Google Scholar 

  56. Zeidler HK (2022) Psoriatic spondylitis: a disease manifestation in debate: evidences to know for the clinical rheumatologist. J Clin Rheumatol 28(1):38–43

    Article  PubMed  Google Scholar 

  57. Benfaremo D, Paci V, Luchetti MM et al (2021) Novel therapeutic approaches and treatment targets for psoriatic arthritis. Curr Pharm Biotechnol 22(1):85–98

    Article  CAS  PubMed  Google Scholar 

  58. Blair HA (2021) Secukinumab: a review in moderate to severe pediatric plaque psoriasis. Paediatr Drugs 23(6):601–608

    Article  PubMed  PubMed Central  Google Scholar 

  59. Bai F, Li GG, Liu Q et al (2019) Short-term efficacy and safety of IL-17, IL-12/23, and IL-23 inhibitors Brodalumab, Secukinumab, Ixekizumab, Ustekinumab, Guselkumab, Tildrakizumab, and Risankizumab for the treatment of moderate to severe plaque psoriasis: a systematic review and network meta-analysis of randomized controlled trials. J Immunol Res 2019:2546161

    Article  PubMed  PubMed Central  Google Scholar 

  60. Yanase T, Tsuruta N, Yamaguchi K et al (2023) Survival rates of systemic interventions for psoriasis in the Western Japan Psoriasis Registry: a multicenter retrospective study. J Dermatol 50(6):753–765

    Article  PubMed  Google Scholar 

  61. Luo Q, Liu Y, Shi K et al (2023) An autonomous activation of interleukin-17 receptor signaling sustains inflammation and promotes disease progression. Immunity 56:2006–20

    Article  CAS  PubMed  Google Scholar 

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Acknowledgements

The authors would like to thank the colleague of Dr. Yanbing Su for technical support.

Funding

We gratefully acknowledge financial support from the Fundamental Research Program of Shanxi Province (No. 202203021222346) and Science Fundation of Shanxi Health Commission (No. 2023ZYYB026).

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Liyun Zhang conceived and directed the study. Minglu Li contributed to literature search. Wenxia Yan designed and analyzed the data and wrote the manuscript.

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Correspondence to Liyun Zhang.

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Yan, W., Li, M. & Zhang, L. Bibliometric analysis on the structure and function of IL17. Egypt Rheumatol Rehabil 51, 23 (2024). https://doi.org/10.1186/s43166-023-00236-3

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