A comprehensive review of IL‐26 to pave a new way for a profound understanding of the pathobiology of cancer, inflammatory diseases and infections

Shabgah, Arezoo Gowhari; Abdelbasset, Walid Kamal; Rahman, Heshu Sulaiman; Bokov, Dmitry Olegovich; Suksatan, Wanich; Thangavelu, Lakshmi; Ahmadi, Majid; Malekahmadi, Mahsa; Gheibihayat, Seyed Mohammad; Navashenaq, Jamshid Gholizadeh

doi:10.1111/imm.13424

Cited by 11 publications

(9 citation statements)

References 76 publications

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“…Immunohistochemical results of AIH liver specimens confirm a significant accumulation of IL‐26 spatially distributed in liver portal areas and lesions of interface hepatitis. Studies have revealed the multiple cellular sources of IL‐26, including T cells, natural killer (NK) cells, NKp30 + γδT cells, CD68 + macrophages and, more recently, lung mucosal‐associated invariant T (MAIT) cells 31,33,34 . In our study, in situ confocal staining speculated that CD4 + T cells, CD8 + T cells and CD68 + macrophages in AIH represent hepatic reservoirs of IL‐26.…”

Section: Discussionmentioning

confidence: 71%

“…17,21,22 For instance, exogenous IL-26 injection augmented Th2-like immune response in the oxazoloneinduced atopic dermatitis murine model 22 and IL-26-induced Th17-type inflammation exacerbated murine sepsis. 30 In contrast with the view that IL-26 is related to disease progression, 31 a pioneer study revealed the therapeutic implication of IL-26. 32 Dextran sodium sulfate (DSS)challenged humanized IL-26 transgenic (hIL-26Tg) mouse exhibited lower inflammatory score and was henceforth protected from acute colitis.…”

Section: Discussionmentioning

confidence: 99%

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IL‐26 modulates T cell function in autoimmune hepatitis

Qian

Liu

et al. 2023

J of Digest Diseases

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Objectives: Autoimmune hepatitis (AIH) is an aberrant autoimmune condition mediated by T cell abnormality, which may cause fulminant liver failure and persistent liver injury. This study aimed to disclose the histopathological and functional engagement of interleukin (IL)-26, a potent inflammation mediator, in AIH disease progression. Methods: We conducted immunohistochemical staining on liver biopsy samples to evaluate intrahepatic expression of IL-26. Cellular sources of hepatic IL-26 were detected by confocal microscopy. Flow cytometry was employed to determine the immunological alterations of CD4 + and CD8 + T cells following in vitro IL-26 treatment on primary peripheral blood mononuclear cells from healthy controls. Results: Statistically significant increase in IL-26 level was observed in AIH (n = 48) liver samples in comparison with patients having chronic hepatitis B (n = 25), nonalcoholic fatty liver disease (n = 18), and healthy donors for living donor liver transplantation (n = 10). The number of intrahepatic IL-26 + cells was positively correlated with histological and serological severity. An immunofluorescence staining indicated that liver-infiltrating CD4 + T cells, CD8 + T cells, and CD68 + macrophages orchestrated IL-26 secretion in AIH. Both CD4 + and CD8 + T cells demonstrated effective activation, lytic, and proinflammatory functions upon IL-26 stimulation. Conclusion: We observed elevated IL-26 in AIH liver which promoted T cell activation and cytotoxic capacity, indicating a therapeutic potential of IL-26 intervention in AIH.

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Section: Discussionmentioning

confidence: 71%

Section: Discussionmentioning

confidence: 99%

IL‐26 modulates T cell function in autoimmune hepatitis

Qian

Liu

et al. 2023

J of Digest Diseases

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“…IL-26 directly binds neutrophil-derived extracellular DNA to facilitate intracellular inflammation signaling in a stimulator of interferon genes (STING)- and inflammasome-dependent manner ( 5 ). It is possible that an enhanced neutrophilic immune response through IL-26 after the vaccination may have been responsible for the ANCA-associated glomerulonephritis in our case.…”

Section: Discussionmentioning

confidence: 99%

“…AAV is a multisystem autoimmune disease, with neutrophil extracellular traps (NETs) involved in its pathogenesis ( 4 ). Interleukin (IL)-26 is a member of the IL-10 family of cytokines that participates in inflammatory signaling through directly binding DNA to facilitate cellular transduction and intracellular inflammation signaling ( 5 ). Recently, it has been shown that IL-26 binds to NETs to induce the secretion of inflammatory cytokines (IL-1β and IL-6) and chemokines (IL-8) by myeloid cells in ANCA-associated glomerulonephritis ( 6 ).…”

Section: Introductionmentioning

confidence: 99%

Anti-glomerular Basement Membrane Disease Concomitant with MPO-ANCA Positivity Concurrent with High Serum Levels of Interleukin-26 Following Coronavirus Disease 2019 Vaccination

et al. 2023

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As coronavirus disease 2019 (COVID-19) vaccine booster campaigns progress worldwide, new reports of complications following COVID-19 vaccination have emerged. We herein report a case of new-onset antiglomerular basement membrane (GBM) disease concomitant with myeloperoxidase-antineutrophil cytoplasmic antibody positivity concurrent with high levels of interleukin (IL)-26 following the second dose of the Pfizer-BioNTech COVID-19 vaccine. The temporal association with vaccination in this case suggests that an enhanced neutrophilic immune response through IL-26 may have triggered necrotizing glomerulonephritis and a T-cell-mediated immune response to GBMs, leading to the development of anti-GBM antibodies, with an enhanced B-cell response after the vaccination triggering anti-GBM IgG and the onset of anti-GBM disease.

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“…Consistent with a classification based on the similarity of receptor compartments and structures, cytokines are divided into four major groups: (i) type I cytokines (comprised of interleukins (IL)-2, IL-3, IL-4, IL-5, IL-6, IL-7, IL-8, IL-9, IL-11, IL-12, IL-13, and IL-15), (ii) type II cytokines (including interferons (IFNs) and the IL-10 superfamily), (iii) tumor necrosis factor (TNF) superfamily (TNFs, Fas ligands, etc. ), and (iv) immunoglobulin (Ig) superfamily (IL-1/IL-18) [ 3 , 4 ].…”

Section: Introductionmentioning

confidence: 99%

IL-26 in the Lung and Its Role in COPD Inflammation

Bartziokas

Fouka

Loukides

et al. 2022

JPM

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IL-26 is a cytokine expressed by infiltrating pro-inflammatory IL-17-producing T cells in the tissues of patients with chronic lung inflammation. IL-26 induces the chemotactic response of human neutrophils to bacteria and other inflammatory stimuli. In recent years, the innovative properties of IL-26 have been described. Studies have shown that, as DNA is released from damaged cells, it binds to IL-26, which plays the role of a carrier molecule for extracellular DNA, further contributing to its binding to the site of inflammation. This mechanism of action indicates that IL-26 may serve both as a driver as well as a stimulus of the inflammatory process, leading to the installation of a noxious amplification loop and, eventually, persistent inflammation. IL-26 also demonstrates direct antimicrobial effects derived from its capability to create pores and disrupt bacterial membranes, as indicated by the presence of membrane blebs on the surface of the bacteria and cytosolic leakage pores in bacterial walls, produced in response to microbial stimuli in human airways by several different immune and structural cells. Surprisingly, while this particular cytokine induces the gathering of neutrophils in areas of infection, it also exhibits inhibitory and pro-inflammatory effects on airway epithelial and immune cells. These remarkable effects underline the necessity of a better understating of its biological behavior and its role in the pathophysiology and disease burden in several smoking-related airway inflammatory disorders, such as Chronic Obstructive Pulmonary Disease (COPD) and chronic bronchitis. In this review, we aim to discuss the current role of IL-26 in the lung, with an emphasis on systemic inflammation in patients suffering from COPD and chronic bronchitis.

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A comprehensive review of IL‐26 to pave a new way for a profound understanding of the pathobiology of cancer, inflammatory diseases and infections

Cited by 11 publications

References 76 publications

IL‐26 modulates T cell function in autoimmune hepatitis

IL‐26 modulates T cell function in autoimmune hepatitis

Anti-glomerular Basement Membrane Disease Concomitant with MPO-ANCA Positivity Concurrent with High Serum Levels of Interleukin-26 Following Coronavirus Disease 2019 Vaccination

IL-26 in the Lung and Its Role in COPD Inflammation

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