Interleukin-29 and interleukin-28A induce migration of neutrophils in rheumatoid arthritis

Xu, Tianyang; Jia, S.; Li, Ping

doi:10.1007/s10067-020-05211-3

Cited by 8 publications

(6 citation statements)

References 23 publications

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“…IL-29 is elevated in the serum of RA patients and participates in the chemotaxis of peripheral blood neutrophils, inhibits T follicular helper (Tfh) cell differentiation by reducing STAT3/BCL6 activity, and induces RANKL expression in FLSs through the MAPK pathway to participate in bone destruction. IL-29 upregulates the levels of TLRs in FLS to mediate the expression of IL-6 and IL-8, which promotes inflammation (178)(179)(180)(181)(182). IL-18 levels in the synovium and serum are related to RA disease activity.…”

Section: Interaction Of Cell Subsets and Cytokines In Rheumatoid Arthritismentioning

confidence: 99%

Molecular and Cellular Heterogeneity in Rheumatoid Arthritis: Mechanisms and Clinical Implications

et al. 2021

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Rheumatoid arthritis is an autoimmune disease that exhibits significant clinical heterogeneity. There are various treatments for rheumatoid arthritis, including disease-modifying anti-rheumatic drugs (DMARDs), glucocorticoids, non-steroidal anti-inflammatory drugs (NSAIDs), and inflammatory cytokine inhibitors (ICI), typically associated with differentiated clinical effects and characteristics. Personalized responsiveness is observed to the standard treatment due to the pathophysiological heterogeneity in rheumatoid arthritis, resulting in an overall poor prognosis. Understanding the role of individual variation in cellular and molecular mechanisms related to rheumatoid arthritis will considerably improve clinical care and patient outcomes. In this review, we discuss the source of pathophysiological heterogeneity derived from genetic, molecular, and cellular heterogeneity and their possible impact on precision medicine and personalized treatment of rheumatoid arthritis. We provide emphasized description of the heterogeneity derived from mast cells, monocyte cell, macrophage fibroblast-like synoviocytes and, interactions within immune cells and with inflammatory cytokines, as well as the potential as a new therapeutic target to develop a novel treatment approach. Finally, we summarize the latest clinical trials of treatment options for rheumatoid arthritis and provide a suggestive framework for implementing preclinical and clinical experimental results into clinical practice.

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Section: Interaction Of Cell Subsets and Cytokines In Rheumatoid Arthritismentioning

confidence: 99%

Molecular and Cellular Heterogeneity in Rheumatoid Arthritis: Mechanisms and Clinical Implications

et al. 2021

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“…IL‐28A cytokines have significant antiviral functions and play different roles across various diseases. For example, IL‐28A levels are significantly increased in patients with rheumatoid arthritis, with obvious chemotaxis of neutrophils in the peripheral blood of afflicted patients 51,52 . Previously, a recombinant adenovirus expressing IL‐28A was directly injected into an A549 lung cancer tumor model, and the results showed that cytokines played an anti‐tumor role by inducing the activation of NK and CD8 + T cells, 53 indicating that IL‐28A has a significant anti‐cancer effect.…”

Section: Discussionmentioning

confidence: 99%

“…For example, IL-28A levels are significantly increased in patients with rheumatoid arthritis, with obvious chemotaxis of neutrophils in the peripheral blood of afflicted patients. 51,52 Previously, a recombinant adenovirus expressing IL-28A was directly injected into an A549 lung cancer tumor model, and the results showed that cytokines played an anti-tumor role by inducing the activation of NK and CD8 + T cells, 53 indicating that IL-28A has a significant anti-cancer effect. Another study established an IL-28A transgenic mouse model of Con A-induced immune liver injury, which exhibited promotion of the recruitment of CD4 + T cells and aggravation of pathological liver damage 28 ; however, the exact mechanism(s) by which IL-28A aggravates acute liver injury remains unclear.…”

Section: Discussionmentioning

confidence: 99%

Interleukin 28A aggravates Con A‐induced acute liver injury by promoting the recruitment of M1 macrophages

Zhang,

Cheng,

Zhang

et al. 2024

The FASEB Journal

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Immune‐mediated acute hepatic injury is characterized by the destruction of a large number of hepatocytes and severe liver function damage. Interleukin‐28A (IL‐28A), a member of the IL‐10 family, is notable for its antiviral properties. However, despite advances in our understanding of IL‐28A, its role in immune‐mediated acute injury remains unclear. The present study investigated the role of IL‐28A in concanavalin A (Con A)‐induced acute immune liver injury. After Con A injection in mice, IL‐28A level significantly increased. IL‐28A deficiency was found to protect mice from acute liver injury, prolong survival time, and reduce serum aspartate aminotransferase and alanine aminotransferase levels. In contrast, recombinant IL‐28A aggravated liver injury in mice. The proportion of activated M1 macrophages was significantly lower in the IL‐28A‐deficiency group than in the wild‐type mouse group. In adoptive transfer experiments, M1 macrophages from WT could exacerbate mice acute liver injury symptoms in the IL‐28A deficiency group. Furthermore, the expression of proinflammatory cytokines, including tumor necrosis factor‐α (TNF‐α), IL‐12, IL‐6, and IL‐1β, by M1 macrophages decreased significantly in the IL‐28A‐deficiency group. Western blotting demonstrated that IL‐28A deficiency could limit M1 macrophage polarization by modulating the nuclear factor (NF)‐κB, mitogen‐activated protein kinase (MAPK), and interferon regulatory factor (IRF) signaling pathways. In summary, IL‐28A deletion plays an important protective role in the Con A‐induced acute liver injury model and IL‐28A deficiency inhibits the activation of M1 macrophages by inhibiting the NF‐κB, MAPK, and IRF signaling pathways. These results provide a potential new target for the treatment of immune‐related hepatic injury.

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“…• RA patients had higher IFN-λ1 mRNA levels in peripheral blood mononuclear cells and higher serum levels of IFN-λ1 in comparison with healthy controls, or non-RA subjects (SLE, SSc, osteoarthritis and fibromyalgia) [96]. • Serum IFN-λ1 levels showed no significant correlation with RA disease activity [97].…”

Section: Rheumatoid Arthritismentioning

confidence: 94%

The Role of Type III Interferons in Human Disease

Malik

Issekutz

2021

CIM

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Purpose: This literature review summarizes the main immunological characteristics of type III interferons (IFN) and highlights the clinically relevant aspects and future therapeutic perspectives for these inflammatory molecules. Source: Relevant articles in PubMed MEDLINE from the first publication (2003) until 2020. N=101 articles were included in this review. Principal findings: Type III IFNs represent a relatively newly described inflammatory cytokine family. Although they induce substantially similar signalling to the well-known type I IFNs, significant functional differences make these molecules remarkable. Type III IFNs have extensive biological effects, contributing to the pathogenesis of several diseases and also offering new diagnostic and therapeutic approaches: 1) their potent anti-viral properties make them promising therapeutics against viral hepatitis and even against severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), which is causing the current coronavirus disease 2019 (COVID-19) pandemic; 2) imbalances in the IFN-λs contribute to several forms of chronic inflammation (e.g., systemic and organ-specific autoimmune diseases) and potentially predict disease progression and therapeutic response to biologic therapies; and 3) the antitumor properties of the type III IFNs open up new therapeutic perspectives against malignant diseases. Conclusion: Over the last 18 years, researchers have gathered extensive information about the presence and role of these versatile inflammatory cytokines in human diseases, but further research is needed to clarify the mechanistic background of those observations. Better understanding of their biological activities will permit us to use type III IFNs more efficiently in new diagnostic approaches and individualized therapies, consequently improving patient care.

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Interleukin-29 and interleukin-28A induce migration of neutrophils in rheumatoid arthritis

Cited by 8 publications

References 23 publications

Molecular and Cellular Heterogeneity in Rheumatoid Arthritis: Mechanisms and Clinical Implications

Molecular and Cellular Heterogeneity in Rheumatoid Arthritis: Mechanisms and Clinical Implications

Interleukin 28A aggravates Con A‐induced acute liver injury by promoting the recruitment of M1 macrophages

The Role of Type III Interferons in Human Disease

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