Synergism between tumor necrosis factor alpha and interleukin-17 to induce IL-23 p19 expression in fibroblast-like synoviocytes

Goldberg, Michael R.; Nadiv, Orna; Luknar-Gabor, N.; Agar, Gabriel; Beer, Yiftah; Katz, Yitzhak

doi:10.1016/j.molimm.2009.01.004

Cited by 49 publications

(38 citation statements)

References 28 publications

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“…Regarding IL-23, in agreement with previous reports, TNFα and IL-17 mediated upregulation of this cytokine [45] as well as a synergistic effect of IL-23 expression after treatment with TNFα plus IL-17 [31,47] in RA-FLS. This synergy has also been described in other proinflammatory mediators such as IL-6 and CXCL8, and could be explained, at least in part, by IL-17-induced mRNA stability of these genes and TNF receptor overexpression [5].…”

Section: Discussionsupporting

confidence: 90%

Inflammatory Mediators Alter Interleukin-17 Receptor, Interleukin-12 and -23 Expression in Human Osteoarthritic and Rheumatoid Arthritis Synovial Fibroblasts: Immunomodulation by Vasoactive Intestinal Peptide

Carrión

Pérez‐García

Jimeno

et al. 2013

Neuroimmunomodulation

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Aims: To assess the contribution of fibroblast-like synoviocytes (FLS) to the inflammatory joint microenvironment under different pathogenic stimuli and their potential to respond to interleukin (IL)-17 and to determine whether the neuroimmunomodulatory vasoactive intestinal peptide (VIP) is able to modulate IL-17 receptor (IL-17R) and related cytokines. Methods: The effect of proinflammatory cytokines [tumor necrosis factor α (TNFα) and IL-17] and Toll-like receptor (TLR) ligands [poly(I:C) and lipopolysaccharide (LPS)] on IL-17R expression and IL-12 and IL-23 production was studied in osteoarthritis (OA)- and rheumatoid arthritis (RA)-FLS, involved in Th1/Th17 differentiation. The effect of VIP was also determined. IL-17RA, IL-17RC, IL-12p35 and IL-23p19 expression was measured by real-time polymerase chain reaction. IL-12 and IL-23 protein levels were measured by ELISA in supernatant cultures. Results: TNFα, LPS and poly(I:C) induced an increase in IL-17RA in RA-FLS, whereas TNFα, TNFα plus IL-17 and poly(I:C) enhanced IL-17RC transcripts in FLS. VIP diminished the upregulated expression of IL-17RA in RA-FLS following TNFα and poly(I:C). TNFα, LPS and poly(I:C) increased IL-12 and IL-23 levels in cells derived from patients presenting both pathologies. However, IL-17A decreased IL-12 and augmented IL-23. VIP decreased IL-12p35 mRNA upregulation by poly(I:C) and IL-23p19 transcripts in LPS-treated FLS. Conclusions: Inflammatory cytokines and TLR ligands modulate IL-17R, IL-12 and IL-23 possibly favoring the cross talk between FLS and Th1/Th17 cells. The ability of VIP to counteract the enhancing effect of proinflammatory molecules on IL-17R and the IL-12 family of cytokines corroborates and amplifies the beneficial effect of this endogenous neuroimmunopeptide in rheumatic diseases.

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Section: Discussionsupporting

confidence: 90%

Inflammatory Mediators Alter Interleukin-17 Receptor, Interleukin-12 and -23 Expression in Human Osteoarthritic and Rheumatoid Arthritis Synovial Fibroblasts: Immunomodulation by Vasoactive Intestinal Peptide

Carrión

Pérez‐García

Jimeno

et al. 2013

Neuroimmunomodulation

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“…TNF-␣ and IL-17A coexpression has been reported previously and found to act in synergy by promoting IL-23p19 and IL-6 expression, the latter through synergistic activation of transcription factors belonging to the C/EBP family (19,44). Further, TNF-␣ has been shown to increase the expression of CD54 (ICAM-1), which would allow CCR6-positive Th17 cells to extravasate at mucosal sites such as the lung through engagement with CCL20 (MIP-3␣) (18).…”

Section: Discussionmentioning

confidence: 65%

Vaccine-Induced Th17 Cells Are Maintained Long-Term Postvaccination as a Distinct and Phenotypically Stable Memory Subset

et al. 2012

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Th17 cells are increasingly being recognized as an important T helper subset for immune-mediated protection, especially against pathogens at mucosal ports of entry. In several cases, it would thus be highly relevant to induce Th17 memory by vaccination. Th17 cells are reported to exhibit high plasticity and may not stably maintain their differentiation program once induced, questioning the possibility of inducing durable Th17 memory. Accordingly, there is no consensus as to whether Th17 memory can be established unless influenced by continuous Th17 polarizing conditions. We have previously reported (T. Lindenstrøm, et al., J. Immunol. 182:8047-8055, 2009) that the cationic liposome adjuvant CAF01 can prime both Th1 and Th17 responses and promote robust, long-lived Th1 memory. Here, we demonstrate that subunit vaccination in mice with CAF01 leads to establishment of bona fide Th17 memory cells. Accordingly, Th17 memory cells exhibited lineage stability by retaining both phenotypic and functional properties for nearly 2 years. Antigen-specific, long-term Th17 memory cells were found to be mobilized from lungdraining lymph nodes to the lung following an aerosol challenge by Mycobacterium tuberculosis nearly 2 years after their induction and proliferated at levels comparable to those of Th1 memory cells. During the infection, the vaccine-induced Th17 memory cells expanded in the lungs and adapted Th1 characteristics, implying that they represent a metastable population which exhibits plasticity when exposed to prolonged Th1 polarizing, inflammatory conditions such as those found in the M. tuberculosis-infected lung. In the absence of overt inflammation, however, stable bona fide Th17 memory can indeed be induced by parenteral immunization.

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“…Low levels of TGF-β synergize with IL-6 to induce Th17 differentiation, whereas high levels of TGF-β result in development of Foxp3 + regulatory T cells [62]. Furthermore, IL-17 and TNF-α have been shown to induce IL-6 and IL-23 expression in synovial fibroblast [63]. These findings could suggest that TGF-β regulates osteoclast genesis by controlling Th17 differentiation.…”

Section: Introductionmentioning

confidence: 99%

TGF-beta1 on osteoimmunology and the bone component cells

2013

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TGF-β1 is an immunoregulatory cytokine that regulates immune cell proliferation, survival, differentiation, and migration. Compelling evidence has demonstrated a strong association between the immune and skeletal systems (so called Osteoimmunology), such as the critical role of TGF-β1 in the development and maintenance of the skeletal tissue. This review provides an overview of the mechanisms in which TGF-β1 interacts with bone component cells, such as osteoblasts, osteoclasts, chondrocytes, mesenchymal stem cells, and hematopoietic stem cells, in concert with other cytokines and hormones.

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Synergism between tumor necrosis factor alpha and interleukin-17 to induce IL-23 p19 expression in fibroblast-like synoviocytes

Cited by 49 publications

References 28 publications

Inflammatory Mediators Alter Interleukin-17 Receptor, Interleukin-12 and -23 Expression in Human Osteoarthritic and Rheumatoid Arthritis Synovial Fibroblasts: Immunomodulation by Vasoactive Intestinal Peptide

Inflammatory Mediators Alter Interleukin-17 Receptor, Interleukin-12 and -23 Expression in Human Osteoarthritic and Rheumatoid Arthritis Synovial Fibroblasts: Immunomodulation by Vasoactive Intestinal Peptide

Vaccine-Induced Th17 Cells Are Maintained Long-Term Postvaccination as a Distinct and Phenotypically Stable Memory Subset

TGF-beta1 on osteoimmunology and the bone component cells

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