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Artykuły w czasopismach na temat „Anti-IL-23”

Autor: Grafiati

Data publikacji: 2 czerwca 2025

Data aktualizacji: 31 lipca 2025

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1

Schwartz, David. "Anti-IL-12/23." Inflammatory Bowel Diseases 15, no. 12 (2009): 1927–28. http://dx.doi.org/10.1002/ibd.20990.

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Gras, J. "Guselkumab. Anti-IL-23 antibody, Antipsoriatic." Drugs of the Future 42, no. 2 (2017): 81. http://dx.doi.org/10.1358/dof.2017.042.02.2564098.

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Held, Katherine, William Glass, Yevgeniya Orlovsky, et al. "Generation of a protective T cell response following viral infection of the CNS is independent of either IL-12 or IL-23 (B141)." Journal of Immunology 178, no. 1_Supplement (2007): LB29. http://dx.doi.org/10.4049/jimmunol.178.supp.b141.

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Abstract The functional role of IL-12 and IL-23 in generating effector T cells following viral infection of the central nervous system (CNS) was determined. Instillation of mouse hepatitis virus (MHV) into the CNS of C57BL/6 mice results in an acute encephalitis followed by a chronic demyelinating disease. MHV-infected mice express mRNA transcripts specific for IL-12p35 and IL-23p19 subunits within the brains. Antibody-mediated blocking of IL-23 (anti-IL-23p19) or IL-12 and IL-23 (anti-IL-12/23p40) did not reduce numbers of virus-specific T cells and treated mice cleared virus from the CNS dem

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4

Brod, Staley A. "Ingested (oral) anti-IL-12/23 inhibits EAE." Journal of the Neurological Sciences 361 (February 2016): 19–25. http://dx.doi.org/10.1016/j.jns.2015.12.011.

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Wendling, Daniel, Clément Prati, Mickael Chouk, and Frank Verhoeven. "Effects of anti-IL-23 and anti-IL-17: The hidden side of spondyloarthritis polymorphism?" Joint Bone Spine 87, no. 1 (2020): 5–7. http://dx.doi.org/10.1016/j.jbspin.2019.06.012.

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Cao, Hao, Qin Lan, Qian Shi, et al. "Anti-IL-23 antibody blockade of IL-23/IL-17 pathway attenuates airway obliteration in rat orthotopic tracheal transplantation." International Immunopharmacology 11, no. 5 (2011): 569–75. http://dx.doi.org/10.1016/j.intimp.2010.11.007.

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Hamada, Kaoru, Yu Sawada, Ryosuke Hino, and Motonobu Nakamura. "HTLV-1 carrier psoriasis patients treated by anti-IL-23/IL-17." Australasian Journal of Dermatology 59, no. 2 (2017): e154-e154. http://dx.doi.org/10.1111/ajd.12701.

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Kyttaris, Vasileios C., Ourania Kampagianni, and George C. Tsokos. "Treatment with Anti-Interleukin 23 Antibody Ameliorates Disease in Lupus-Prone Mice." BioMed Research International 2013 (2013): 1–5. http://dx.doi.org/10.1155/2013/861028.

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Interleukin 23 receptor expressing IL-17 producing T cells have been shown to be important in the development of murine lupus. The usefulness of IL-23 inhibition in ameliorating lupus nephritis is unknown. We hypothesized that inhibition of IL-23 will ameliorate nephritis in lupus-prone mice. To this end, we treated MRL/lprlupus-prone mice for 6 weeks with a rat anti-IL-23p19 antibody, which resulted in delaying the onset of nephritis without affecting the production of anti-dsDNA antibodies. The effect of the treatment was hampered by the production of murine anti-rat IgG antibodies. The amel

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9

Alhasani, Salam, and Nasser Yousif. "Critical role of IL-23 signaling in prostatic cancer." American Journal of BioMedicine 1, no. 1 (2013): 4–6. http://dx.doi.org/10.18081/ajbm/2333-5106-013-11/4-6.

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Interleukin 23 (IL-23) belongs to interleukin 6 super-family [1]. IL-12/23 p40 is the common subunit for them, which is covalently linked to either a p19 subunit to form IL-23 or a p35 subunit to form IL-12 [2]. Both cytokines are mainly expressed by activating dendrite cells or macrophages under the stimulation of pathogens. IL-23 was also reported to be secreted by tumor associated macrophages in tumor microenvironment [3]. Interestingly, IL-23 spur different immune pathways [4]. IL-12 induces IFN-γ-producing Th1 cell development and enhances cytotoxic, anti-microbial and anti-tumor response

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10

Whitley, Sarah K., Mushi Li, Tracy Tabib, et al. "IL-23 maintains tissue resident memory Th17 cells in murine and psoriatic skin." Journal of Immunology 206, no. 1_Supplement (2021): 98.50. http://dx.doi.org/10.4049/jimmunol.206.supp.98.50.

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Abstract Tissue resident memory Th17 cells (TRM17) are the key cell type driving the chronic skin inflammation of psoriasis. Although IL-23 is strongly associated with autoimmunity and chronic inflammatory disorders including psoriasis, and anti-IL-23 biologic agents have remarkable efficacy in the treatment of psoriasis, the precise role of IL-23 in supporting IL-17-mediated skin inflammation remains unclear. In mice, we found that circulating memory T cells were dispensable for anamnestic protection from C. albicans skin infection, and TRM17 mediated protection from C. albicans reinfection r

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11

Hao, Jing-Sheng, and Bao-En Shan. "Immune enhancement and anti-tumour activity of IL-23." Cancer Immunology, Immunotherapy 55, no. 11 (2006): 1426–31. http://dx.doi.org/10.1007/s00262-006-0171-5.

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12

Ranzinger, D., J. Thomas, A. C. Pilz, P. Seiringer, S. Eyerich, and K. Eyerich. "045 Anti-IL-23 preferentially inhibits pathogenic TH17 cells." Journal of Investigative Dermatology 143, no. 5 (2023): S8. http://dx.doi.org/10.1016/j.jid.2023.03.046.

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13

Blauvelt, Andrew, Mark G. Lebwohl, and Robert Bissonnette. "IL-23/IL-17A Dysfunction Phenotypes Inform Possible Clinical Effects from Anti-IL-17A Therapies." Journal of Investigative Dermatology 135, no. 8 (2015): 1946–53. http://dx.doi.org/10.1038/jid.2015.144.

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14

Leong, Xue Bin, Chuan Zhe Tang, Chloe Zi Ying Lee, Zoe Ling Hui Lee, and Thai Hau Koo. "Comparative Role of Anti-TNF Agents versus IL-12/23 Inhibitors in Inflammatory Bowel Disease: An Updated Review." Indonesian Journal of Gastroenterology, Hepatology, and Digestive Endoscopy 25, no. 3 (2024): 57–61. https://doi.org/10.24871/253202457-61.

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Treatments for Crohn's Disease (CD) and Ulcerative Colitis (UC), two conditions that fall under the umbrella of Inflammatory Bowel Disease (IBD), must be both safe and effective. This review compares the effectiveness and safety of anti-TNF agents and IL-12/23 inhibitors, specifically in the context of IBD management. Randomized controlled trials (RCTs), observational studies, and meta-analyses involving adult IBD patients were all included in the review. Anti-TNF agents (infliximab and adalimumab) were shown to significantly improve clinical remission rates and reduce complications, particula

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15

Miyagawa, Hanae, Hiromichi Hara, Jun Araya, et al. "Characteristics of anti-IL-17/23 biologics-induced interstitial pneumonia in patients with psoriasis." PLOS ONE 16, no. 1 (2021): e0245284. http://dx.doi.org/10.1371/journal.pone.0245284.

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Objectives Anti-IL-17/23 biologics are increasingly used to treat psoriasis. We aimed to elucidate characteristics of drug-induced interstitial pneumonia (DIIP) caused by anti-IL-17/23 biologics. Methods We retrospectively analyzed the clinical data of psoriasis patients treated with anti-IL-17/23 biologics. Chest CT was performed to evaluate DIIP. Serum KL-6 levels were measured before treatment (baseline) and during treatment. Results A total of 603 psoriasis patients were treated with anti-IL-17/23 biologics with mean follow-up of 21.1 months. Six patients developed DIIP at mean 14 months a

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16

Yago, Toru, Yuki Nanke, Manabu Kawamoto, et al. "IL-23 induces human osteoclastogenesis via IL-17 in vitro, and anti-IL-23 antibody attenuates collagen-induced arthritis in rats." Arthritis Research & Therapy 9, no. 5 (2007): R96. http://dx.doi.org/10.1186/ar2297.

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17

Lee, Hyun Seung, Da-Eun Park, Ji-Won Lee, et al. "IL-23 secreted by bronchial epithelial cells contributes to allergic sensitization in asthma model: role of IL-23 secreted by bronchial epithelial cells." American Journal of Physiology-Lung Cellular and Molecular Physiology 312, no. 1 (2017): L13—L21. http://dx.doi.org/10.1152/ajplung.00114.2016.

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IL-23 has been postulated to be a critical mediator contributing to various inflammatory diseases. Dermatophagoides pteronyssinus (Der p) is one of the most common inhalant allergens. However, the role of IL-23 in Der p-induced mouse asthma model is not well understood, particularly with regard to the development of allergic sensitization in the airways. The objective of this study was to evaluate roles of IL-23 in Der p sensitization and asthma development. BALB/c mice were repeatedly administered Der p intranasally to develop Der p allergic sensitization and asthma. After Der p local adminis

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18

Matteo, Auriemma, Caponio Chiara, Ruggiero Carlo, Giuliani Federica, and Amerio Paolo. "Anti-IL-12/IL-23 treatment for a psoriatic patient with heart failure." International Journal of Case Reports and Images 4, no. 5 (2013): 266. http://dx.doi.org/10.5348/ijcri-2013-05-309-cr-6.

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19

Costa, Luisa, Roberta Ramonda, Augusta Ortolan, et al. "Psoriatic arthritis and obesity: the role of anti-IL-12/IL-23 treatment." Clinical Rheumatology 38, no. 9 (2019): 2355–62. http://dx.doi.org/10.1007/s10067-019-04663-6.

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20

Frieder, Jillian, Dario Kivelevitch, Isabel Haugh, Ian Watson, and Alan Menter. "Anti-IL-23 and Anti-IL-17 Biologic Agents for the Treatment of Immune-Mediated Inflammatory Conditions." Clinical Pharmacology & Therapeutics 103, no. 1 (2017): 88–101. http://dx.doi.org/10.1002/cpt.893.

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21

Wan, Y., M. Zhu, J. Gai, Y. Huang, and Y. Hu. "P0640 Development and characterization of LQ080, a novel extended half-life bispecific TL1A/IL-23 p19 single domain antibody for the treatment of IBD." Journal of Crohn's and Colitis 19, Supplement_1 (2025): i1259. https://doi.org/10.1093/ecco-jcc/jjae190.0814.

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Abstract Background Despite the effectiveness of current anti-TL1A treatments, unmet needs remain for effective therapeutics for IBD. Therapies simultaneously neutralizing TL1A and IL-23 might be better choices owing to their synergistic anti-inflammatory effects in the pathogenesis of IBD. Methods TL1A and IL-23 single domain antibodies (sdAbs) were selected from immunized sdAb Phage display libraries. A human whole blood-based assay measuring IFNγ secretion was used to assess functional blockade of TL1A. Mouse splenocytes based assay measuring mouse IL-17 release was used to evaluate functio

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22

Ho, Ji-Chen, Chih-Hung Lee, and Shang-Hung Lin. "No Significant Reduction of Circulating Endothelial-Derived and Platelet-Derived Microparticles in Patients with Psoriasis Successfully Treated with Anti-IL12/23." BioMed Research International 2016 (2016): 1–6. http://dx.doi.org/10.1155/2016/3242143.

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Psoriasis is associated with atherosclerosis, in which circulating microparticles play an important role. In severe psoriasis, there was an increase of endothelial- and platelet- microparticles which could be decreased by anti-TNFα. However, whether anti-IL-12/23 treatment would decrease the level of microparticles remains unknown. Our study showed that, despite the clinical improvement of psoriasis after IL-12/13 blockage, the increased levels of circulating CD41a and CD31 microparticles were unchanged after anti-IL-12/23. This result suggested that anti-IL12/23 treatment may not alter the de

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23

Li, Yuanteng Jeff, Pavlos Msaouel, Matthew Campbell, Patrick Hwu, Adi Diab, and Sang T. Kim. "Successful management of pre-existing psoriatic arthritis through targeting the IL-23/IL-17 axis in cancer patients receiving immune checkpoint inhibitor therapy: a case series." RMD Open 10, no. 3 (2024): e004308. http://dx.doi.org/10.1136/rmdopen-2024-004308.

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BackgroundImmune checkpoint inhibitors (ICIs) have significantly improved outcomes for patients with cancer. However, these therapies are associated with adverse events including de novo immune-related adverse events or flare of pre-exiting autoimmune disorders. Up to 80% of patients with cancer and pre-existing psoriasis (PsO) or psoriatic arthritis (PsA) experience PsO/PsA flare after initiating ICIs. Targeting the interleukin (IL)-17/IL-23 axis is a mainstream of the PsO/PsA treatment. However, whether this treatment can effectively control PsO/PsA with ICI exposure while preserving anti-tu

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24

Liu, Haiyan, Yonghao Liu, Yuan Song, and Bo Hu. "IL-23 promotes the development of hepatocellular carcinoma through the induction of IL-17-producing ILC3 (TUM10P.1044)." Journal of Immunology 194, no. 1_Supplement (2015): 211.25. http://dx.doi.org/10.4049/jimmunol.194.supp.211.25.

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Abstract IL-23 has been shown to play a pathogenic role in autoimmunity through the promotion of Th17 cells. However, its role in tumor development remains controversial. Some studies demonstrated that IL-23 could activate T cells and NK cells to suppress tumor metastasis and growth. However, it has also been shown to promote tumor growth in colon cancer, lung cancer, breast cancer and melanoma. In the current study, we established a murine hepatocellular carcinoma (HCC) model and found that IL-23 could promote HCC development. The in vitro study demonstrated that IL-23 could directly promote

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25

Cao, S., K. Ma, and P. Deepak. "DOP095 IL-23-activated cells as response biomarkers for risankizumab in Crohn’s disease patients." Journal of Crohn's and Colitis 19, Supplement_1 (2025): i254—i256. https://doi.org/10.1093/ecco-jcc/jjae190.0134.

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Abstract Background The interleukin (IL)-23 signaling is a vital pathway in Crohn’s disease (CD). IL-23 activates T-helper (Th) 17 cells, IL-17-secreting CD8 T (Tc)17 cells, γδ T cells, natural killer (NK) T cells, and group 3 innate lymphoid cells (ILC3) to secrete inflammatory cytokines including IL-17, IFN-γ, and TNF-α. Risankizumab is the first selective IL-23 antagonist approved for moderate-to-severe CD; however, no biomarker currently exists to predict response to this medication. Here, we characterized the phenotypes of IL-23-activated cells that predict response to risankizumab in CD

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Misra, Durga Prasanna, Smriti Chaurasia, and Ramnath Misra. "Increased Circulating Th17 Cells, Serum IL-17A, and IL-23 in Takayasu Arteritis." Autoimmune Diseases 2016 (2016): 1–8. http://dx.doi.org/10.1155/2016/7841718.

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Introduction.Th17,γδT, NK, and NKT cells in peripheral blood and serum IL-17 and IL-23 in Takayasu arteritis (TA) were measured and correlated with disease activity.Methods.Th17 (anti-CD3APC, CD4PECy7, and IL-17PE), NKT, NK (anti-CD3APC, CD56FITC), andγδT (anti-CD3FITC andγδTCRAPC) cells were enumerated by flow cytometry in peripheral blood of 30 patients with TA (ACR1990 criteria) and 20 healthy controls, serum IL-17 and IL-23 measured by ELISA. Relation with disease activity (NIH criteria, ITAS2010) was analyzed (using nonparametric tests, median with interquartile range).Results.Mean age of

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Zhang, Yingli, Rongrong Liang, Aicen Xie, Wenqian Shi, Huarong Huang, and Yingqiang Zhong. "Antagonistic Peptides That Specifically Bind to the First and Second Extracellular Loops of CCR5 and Anti-IL-23p19 Antibody Reduce Airway Inflammation by Suppressing the IL-23/Th17 Signaling Pathway." Mediators of Inflammation 2020 (April 28, 2020): 1–13. http://dx.doi.org/10.1155/2020/1719467.

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Asthma is a heterogeneous chronic inflammatory disorder of the airways with a complex etiology, which involves a variety of cells and cellular components. Therefore, the aim of the study was to investigate the effects and mechanisms of antagonistic peptides that specifically bind to the first and second extracellular loops of CCR5 (GH and HY peptides, respectively) and anti-interleukin-23 subunit p19 (anti-IL-23p19) in the airway and thereby mediate inflammation and the IL-23/T helper 17 (Th17) cell pathway in asthmatic mice. An experimental asthma model using BALB/c mice was induced by ovalbu

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28

Schmitt, Heike, Ulrike Billmeier, Walburga Dieterich, et al. "Expansion of IL-23 receptor bearing TNFR2+ T cells is associated with molecular resistance to anti-TNF therapy in Crohn’s disease." Gut 68, no. 5 (2018): 814–28. http://dx.doi.org/10.1136/gutjnl-2017-315671.

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ObjectiveAnti-tumour necrosis factor (TNF) antibodies are successfully used for treatment of Crohn’s disease. Nevertheless, approximately 40% of patients display failure to anti-TNF therapy. Here, we characterised molecular mechanisms that are associated with endoscopic resistance to anti-TNF therapy.DesignMucosal and blood cells were isolated from patients with Crohn’s disease prior and during anti-TNF therapy. Cytokine profiles, cell surface markers, signalling proteins and cell apoptosis were assessed by microarray, immunohistochemistry, qPCR, ELISA, whole organ cultures and FACS.ResultsRes

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Li, Hao, Hui-Chen Hsu, Jun Li, et al. "IL-23 induces IRF5 and polarizes inflammatory M1 macrophages to promote inflammation in a mouse model of arthritis (171.5)." Journal of Immunology 188, no. 1_Supplement (2012): 171.5. http://dx.doi.org/10.4049/jimmunol.188.supp.171.5.

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Abstract Increased numbers of macrophages (MΦs) is an early hallmark of active arthritis. Expression of IL-23R has been identified on myeloid cells. We determined if IL-23 can regulate the pathogenesis of collagen II-induced arthritis (CIA) by directly modulating development of MΦs. AdIL-17 was injected to Il23p19-/- and Il23p19+/+ mice to induce equal levels of IL-17 yet Il23p19-/-mice were more resistant to CIA compared to Il23p19+/+ mice. Dramatic expansion of IL-23R+ MΦs, which are the major producers of IL-6 and TNFα in the draining LN of mice with CIA, occurred only in Il23p19+/+ but not

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Gargiulo, Luigi, Luciano Ibba, Alessandra Narcisi, et al. "Anti-IL-17/23 Drugs for the Treatment of Moderate-to-Severe Hidradenitis Suppurativa in Patients With Concomitant Psoriasis: A Multicenter Retrospective Study." Dermatology Practical & Conceptual 14, no. 4 (2024): e2024250. http://dx.doi.org/10.5826/dpc.1404a250.

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Introduction: Psoriasis and hidradenitis suppurativa (HS) are chronic inflammatory diseases with significant overlap in their immunologic pathways, which involve cytokines such as tumor necrosis factor-alfa, interleukin (IL)-17, and IL-23. Current treatment options for HS are limited, as only adalimumab and secukinumab are approved for severe cases. Given the overlapping pathogenetic features between HS and psoriasis, anti-IL-17 and anti-IL-23 drugs could represent valuable treatments for the management of HS. Objectives: We sought to evaluate the effectiveness and safety of anti-IL-17 and ant

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Feng, Ting, Hongwei Qin, Lanfang Wang, Etty Benveniste, Charles Elson, and Yingzi Cong. "Microbiota antigen specific Th17 cells induce colitis and promote Th1 cell response through IL-17 induction of innate cell IL-12 and IL-23 production (47.3)." Journal of Immunology 184, no. 1_Supplement (2010): 47.3. http://dx.doi.org/10.4049/jimmunol.184.supp.47.3.

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Abstract Both Th1 and Th17 cells have been implicated in the pathogenesis of IBD and experimental colitis. However, the complex relationship between Th1 and Th17 cells has not been completely analyzed. Although it has been shown recently that Th17 cells can convert into Th1 cells, the underlying in vivo mechanisms and the role of Th1 cells converted from Th17 cells in colitis pathogenesis are still largely unknown. By using Thy1.1-IFNγ reporter mice and IL-17 capture technique, we generated Th1 and Th17 cells of high purity from immunodominant microbiota antigen CBir1 flagellin specific TCR tr

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Klune, John R., Christian Bartels, Jing Luo, Shinichiro Yokota, Qiang Du та David A. Geller. "IL-23 mediates murine liver transplantation ischemia-reperfusion injury via IFN-γ/IRF-1 pathway". American Journal of Physiology-Gastrointestinal and Liver Physiology 315, № 6 (2018): G991—G1002. http://dx.doi.org/10.1152/ajpgi.00231.2018.

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Interleukin-23 (IL-23) is a proinflammatory cytokine initially studied in autoimmune disease that has been more recently linked to innate immunity. We observed that the expression of IL-23 is upregulated during hypoxia in a hepatocyte and nonparenchymal cell (NPC) coculture system, as well as during ischemia-reperfusion (I/R) injury in the liver. Interferon regulatory factor-1 (IRF-1) is a transcription factor that induces expression of multiple inflammatory cytokines and has been shown to play a critical role in liver I/R injury. We observed that IL-23 signaling induces not only the IL-17/che

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José, Anthar Ávalos Narváez, Daniel Solís Dittrich Kevin, Elisa González Robles María, Jiménez Zaragoza Michelle, Arturo Ovilla Alvarez Ricardo, and Aréchiga López Mayra. "Advances in Monoclonal Antibody Therapy for Moderate to Severe Psoriasis: Targeting TNF, IL-17, And IL-23 Pathways for Optimal Disease Management." International Journal of Medical Science and Clinical Research Studies 5, no. 05 (2025): 766–69. https://doi.org/10.5281/zenodo.15502235.

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Psoriasis, a chronic immune-mediated dermatological disorder, significantly impacts patients' quality of life, particularly in its moderate to severe forms. The advent of biologic therapies, specifically monoclonal antibodies (mAbs), has revolutionized the treatment landscape. This article provides an in-depth analysis of the efficacy, safety, and mechanistic insights of anti-TNF (e.g., adalimumab, infliximab), anti-IL-17 (e.g., secukinumab, ixekizumab), and anti-IL-23 (e.g., guselkumab, risankizumab) agents in the management of moderate to severe psoriasis. Clinical trials and real-world evid

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Fried, Richard, Mark Lebwohl, Miriam Bettencourt, John Koo, and Abby Jacobson. "Onset of Plaque Psoriasis Treatment Responses With Anti-IL-17/IL-23 Biologic Therapies." Journal of Drugs in Dermatology 21, no. 8 (2022): 854–60. http://dx.doi.org/10.36849/jdd.66791.

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Cao, S., M. Colonna, and P. Deepak. "DOP19 High dimensional profiling of IL-23-responsive cells revealed molecular signatures that predict response to anti-IL-23 therapy in patients with Crohn’s Disease." Journal of Crohn's and Colitis 18, Supplement_1 (2024): i106—i107. http://dx.doi.org/10.1093/ecco-jcc/jjad212.0059.

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Abstract Background The interleukin (IL)-23 signaling plays a crucial role in the pathogenesis of Crohn’s disease (CD). IL-23 activates T-helper (Th) 17 cells, IL-17-secreting CD8 T (Tc)17 cells, gd T cells, nature killer (NK) T cells, and group 3 innate lymphoid cells (ILC3) to secrete proinflammatory cytokines including IL-17, IFN-g, and TNF-a. Risankizumab is the first selective IL-23 antagonist approved for moderate-severe CD. However, there is currently no biomarker to predict response to anti-IL-23 antibodies in IBD. Here, we characterized the cell type- and cytokine-specific pathways in

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Liu, Yonghao, Yuan Song, Lei Lei, Yuhui Huang, and Haiyan Liu. "NCR−ILC3 as the initial responders to liver inflammatory environment promote HCC development through IL-23/IL-17 axis." Journal of Immunology 200, no. 1_Supplement (2018): 122.1. http://dx.doi.org/10.4049/jimmunol.200.supp.122.1.

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Abstract IL-17 is crucial in tumor-promoting inflammation and the development of hepatocellular carcinoma (HCC). However, the role of IL-23, an important IL-17-inducing inflammatory cytokine, as well as the immune cells responsible for initiating IL-17 production in the tumor microenvironment are not clear. In the current study, we assessed the development of HCC and the function of the adaptive anti-tumor immune response, as well as the kinetics of the development of IL-17-producing cells in an IL-23-rich tumor microenvironment. Our results demonstrated that IL-23 promoted HCC tumor growth an

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Fischer, Katarzyna, Hanna Przepiera-Będzak, Marcin Sawicki, Anna Walecka, Iwona Brzosko, and Marek Brzosko. "Serum Interleukin-23 in Polish Patients with Systemic Lupus Erythematosus: Association with Lupus Nephritis, Obesity, and Peripheral Vascular Disease." Mediators of Inflammation 2017 (2017): 1–9. http://dx.doi.org/10.1155/2017/9401432.

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Objectives. To analyze the correlation between the serum concentration of interleukin- (IL-) 23 and atherosclerotic changes, traditional atherosclerotic risk factors, the autoantibody profile, and involvement of selected organs in systemic lupus erythematosus (SLE) patients.Patients and Methods. We studied 94 SLE patients and 27 controls. We analyzed the IL-23 serum concentration, autoantibodies, carotid intima-media thickness and atherosclerotic plaque, the ankle-brachial index, atherosclerotic risk factors, and organ manifestations.Results. Concentrations of IL-23 significantly differed betw

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Quiniou, Christiane, Maria Domínguez-Punaro, Frank Cloutier, et al. "Specific targeting of the IL-23 receptor, using a novel small peptide noncompetitive antagonist, decreases the inflammatory response." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 307, no. 10 (2014): R1216—R1230. http://dx.doi.org/10.1152/ajpregu.00540.2013.

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IL-23 is part of the IL-12 family of cytokines and is composed of the p19 subunit specific to IL-23 and the p40 subunit shared with IL-12. IL-23 specifically contributes to the inflammatory process of multiple chronic inflammatory autoimmune disorders, including psoriasis, multiple sclerosis, inflammatory bowel disease, and rheumatoid arthritis. So far, one antibody targeting the shared p40 subunit of IL-12 and IL-23, Ustekinumab, is approved clinically to treat psoriasis. However, there are no treatments inhibiting specifically the IL-23 proinflammatory response. We have developed small IL-23

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Cao, Siyan, Kaiming Ma, and Parakkal Deepak. "IL-23-ACTIVATED CELLS PREDICT RESPONSE TO RISANKIZUMAB IN CROHN’S DISEASE." Inflammatory Bowel Diseases 31, Supplement_1 (2025): S56—S57. https://doi.org/10.1093/ibd/izae282.135.

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Abstract BACKGROUND & AIMS The interleukin (IL)-23 signaling plays a crucial role in the pathogenesis of Crohn’s disease (CD). IL-23 activates T-helper (Th) 17 cells, IL-17-secreting CD8 T (Tc)17 cells, γδ T cells, nature killer (NK) T cells, and group 3 innate lymphoid cells (ILC3) to secrete proinflammatory cytokines including IL-17, IFN-γ, and TNF-α. Risankizumab is the first selective IL-23 antagonist approved for moderately to severely active CD. However, there is currently no biomarker to predict response to anti-IL-23 antibodies in IBD. Here, we characterized the cell type- and cyto

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Rudner, Xiaowen L., Kyle I. Happel, Erana A. Young, and Judd E. Shellito. "Interleukin-23 (IL-23)-IL-17 Cytokine Axis in Murine Pneumocystis carinii Infection." Infection and Immunity 75, no. 6 (2007): 3055–61. http://dx.doi.org/10.1128/iai.01329-06.

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ABSTRACT Host defense mechanisms against Pneumocystis carinii are not fully understood. Previous work in the murine model has shown that host defense against infection is critically dependent upon host CD4+ T cells. The recently described Th17 immune response is predominantly a function of effector CD4+ T cells stimulated by interleukin-23 (IL-23), but whether these cells are required for defense against P. carinii infection is unknown. We tested the hypothesis that P. carinii stimulates the early release of IL-23, leading to increases in IL-17 production and lung effector CD4+ T-cell populati

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Lyssia, B., M. Caroline, M. Aurore, et al. "DOP031 Anti-IL-7 receptor plus anti-IL12/23 combination induces complete histological normalization in chronic colitis." Journal of Crohn's and Colitis 19, Supplement_1 (2025): i139. https://doi.org/10.1093/ecco-jcc/jjae190.0070.

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Abstract Background The signaling networks perpetuating chronic inflammatory bowel disease remain unclear. Interleukin-7 (IL-7) has been previously reported to trigger the expansion of effector Th17 cells and anti-IL-7 receptor (IL-7R) antagonism to render IL23-differentiated Th17 cells susceptible to apoptosis1. We previously reported that IL-7R pathway is locally dysregulated and over-expressed in the colon mucosa of severe IBD patients and reproducibly associated with unresponsiveness to anti-TNF or anti-α4β7 integrin therapies2. We developed a humanized anti-IL7R lusvertikimab with a good

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Kroenke, Mark A., Thaddeus J. Carlson, Anuska V. Andjelkovic, and Benjamin M. Segal. "IL-12– and IL-23–modulated T cells induce distinct types of EAE based on histology, CNS chemokine profile, and response to cytokine inhibition." Journal of Experimental Medicine 205, no. 7 (2008): 1535–41. http://dx.doi.org/10.1084/jem.20080159.

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The interleukin (IL)-12p40 family of cytokines plays a critical role in the development of experimental autoimmune encephalomyelitis (EAE). However, the relative contributions of IL-12 and IL-23 to the pathogenic process remain to be elucidated. Here, we show that activation of uncommitted myelin-reactive T cells in the presence of either IL-12p70 or IL-23 confers encephalogenicity. Adoptive transfer of either IL-12p70– or IL-23–polarized T cells into naive syngeneic hosts resulted in an ascending paralysis that was clinically indistinguishable between the two groups. However, histological and

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Chu, Yi-Lun, and Sebastian Yu. "Hidradenitis Suppurativa: An Understanding of Genetic Factors and Treatment." Biomedicines 12, no. 2 (2024): 338. http://dx.doi.org/10.3390/biomedicines12020338.

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Hidradenitis suppurativa (HS), recognized as a chronic and debilitating skin disease, presents significant challenges in both diagnosis and treatment. This review explores the clinical manifestations, genetic landscape, and molecular mechanisms underlying HS. The disease’s association with a predisposing genetic background, obesity, smoking, and skin occlusion underscores the complexity of its etiology. Genetic heterogeneity manifests in sporadic, familial, and syndromic forms, with a focus on mutations in the γ-secretase complex genes, particularly NCSTN. The dysregulation of immune mediators

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Ali Shareef, Saja, Risala H. Allami, and Ruqaya M. Al-ezzy. "Correlation between Interleukin-23, Autoantibodies and Thyroid Profile in a Sample of Iraqi Patients with Hashimoto’s Thyroiditis." IOP Conference Series: Earth and Environmental Science 1325, no. 1 (2024): 012024. http://dx.doi.org/10.1088/1755-1315/1325/1/012024.

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Abstract Hashimoto’s thyroiditis (HT) is the most common autoimmune condition characterized by hypothyroidism and thyroid cell death by leukocytes and antibody-mediated immunological mechanisms. The current paper set out to assess a number of inflammatory and metabolic potential indicators of Hashimoto’s thyroiditis. Fifty-one patients with Hashimoto’s thyroiditis took part in the current investigation. Ages ranged from 20 to 75 for them. Enzyme-linked immunosorbent tests were used to quantify the anti-thyroperoxidase antibody (anti-TPO Ab), anti-thyroglobulin antibody (anti-Tg Ab), T4, T3, an

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Hu, Xiaorong, Ruisong Ma, Jiajia Lu, et al. "IL-23 Promotes Myocardial I/R Injury by Increasing the Inflammatory Responses and Oxidative Stress Reactions." Cellular Physiology and Biochemistry 38, no. 6 (2016): 2163–72. http://dx.doi.org/10.1159/000445572.

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Background/Aims: Inflammation and oxidative stress play an important role in myocardial ischemia and reperfusion (I/R) injury. We hypothesized that IL-23, a pro-inflammatory cytokine, could promote myocardial I/R injury by increasing the inflammatory response and oxidative stress. Methods: Male Sprague-Dawley rats were randomly assigned into sham operated control (SO) group, ischemia and reperfusion (I/R) group, (IL-23 + I/R) group and (anti-IL-23 + I/R) group. At 4 h after reperfusion, the serum concentration of lactate dehydrogenase (LDH), creatine kinase (CK) and the tissue MDA concentratio

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Hong, Huixian, Qi Wu, PingAr Yang, et al. "A novel mechanism for IL-23 to up-regulate AICDA and promote pathogenic autoantibodies in lupus." Journal of Immunology 200, no. 1_Supplement (2018): 40.1. http://dx.doi.org/10.4049/jimmunol.200.supp.40.1.

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Abstract Targeting IL-23 to treat autoimmune disease and chronic inflammation is under development based on its proinflammatory function and pro-Th17 cell effects. IL-23 was previously shown to be important for promoting pathogenic autoantibody production in B6-Faslpr/lpr mice. In contrast, the lack of IL-23 did not influence germinal center (GC) formation and IgG anti-CII autoantibodies in type II collagen immunized DBA/1 mice. We determined if IL-23 regulated development of spontaneous GCs and autoantibody production in lupus-prone BXD2 mice by generating IL-23 deficient BXD2-p19−/− mice. Th

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Yoshida, Hiroki, Yoshiyuki Miyazaki, Sen Wang, and Shinjiro Hamano. "Regulation of Defense Responses against Protozoan Infection by Interleukin-27 and Related Cytokines." Journal of Biomedicine and Biotechnology 2007 (2007): 1–7. http://dx.doi.org/10.1155/2007/79401.

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Cytokine-mediated immunity is crucial in the defense against pathogens. Recently, IL-23 and IL-27 were identified, which along with IL-12 belong to the IL-12 cytokine family. IL-27 is pivotal for the induction of helper T cell (Th) 1 responses while IL-23 is important for the proliferation of memory type Th1 cells. Recent studies revealed that IL-27 also has an anti-inflammatory property. In some protozoan infection, various proinflammatory cytokines were over produced causing lethal inflammatory responses in IL-27 receptor-deficient mice. The anti-inflammatory effect of IL-27 depends, at leas

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Pang, Dan-Dan, Li Cai, Jing-Ru Zhang, and Sheng-Ming Dai. "IL-23 induces the expression of pro-osteogenic factors in osteoclasts." Aktuelle Rheumatologie 45, no. 05 (2020): 467–74. http://dx.doi.org/10.1055/a-1099-9028.

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Abstract Background The mechanism for the new bone formation in ankylosing spondylitis (AS) is still unclear. Although it has been demonstrated that IL-23 plays a pivotal role in the pathophysiology of AS, IL-23 has no direct effects on osteoblasts but modulates the function of osteoclasts. Aims To explore whether IL-23 indirectly facilitates new bone formation through osteoclasts in AS, here we analyzed whether IL-23 enhances the expression levels of pro-osteogenic factors by osteoclasts. Methods Mononuclear cells were harvested from mouse bone marrow and cultured in the presence of M-CSF (50

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Cairns, J., S. Monkley, S. Tian, et al. "DOP06 Deep characterization of IL-23 pathway in different gut segments and associated plasma biomarkers in inflammatory bowel disease." Journal of Crohn's and Colitis 17, Supplement_1 (2023): i64—i67. http://dx.doi.org/10.1093/ecco-jcc/jjac190.0046.

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Abstract Background The role of Interleukin 23 (IL-23) in the pathogenesis of both Crohn’s disease (CD) and ulcerative colitis (UC) is well documented. However, more than half of patients do not respond or lose response to current anti-IL-23 treatments. Thus, we aimed to identify patients with IL-23-driven disease using gut segment-specific transcriptome analysis and quantification of IL-23 pathway cytokines in plasma to enable patient stratification in inflammatory bowel disease (IBD). Methods Analyses of real-world data from the Study of a Prospective Adult Research Cohort with IBD (SPARC IB

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Lee, Priscilla, Alan Smith, Yuhong Yang, Michael Racke, and Amy Lovett-Racke. "Identifying the cytokines provided by antigen-presenting cells critical for generating an encephalitogenic T cell (BA11P.126)." Journal of Immunology 194, no. 1_Supplement (2015): 184.8. http://dx.doi.org/10.4049/jimmunol.194.supp.184.8.

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Abstract Multiple sclerosis (MS) is a CD4 T cell-mediated demyelinating disease; however, what determines the encephalitogenicity of T cells remains unclear. Recognizing myelin peptides is not sufficient, as the frequencies of myelin-reactive T cells are similar between MS patients and healthy individuals. In experimental autoimmune encephalomyelitis (EAE), anti-CD3/CD28 antibodies-generated myelin-specific T cells do not transfer disease, but antigen-presenting cells (APC)-generated ones do. This suggests that the cytokines secreted by APC provide critical signals beyond T cell receptor activ

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