Recent advances in the IL-17 cytokine family

doi:10.1016/J.COI.2011.07.006

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Recent advances in the IL-17 cytokine family

Journal Article•DOI•

Recent advances in the IL-17 cytokine family

Sarah L. Gaffen¹•Institutions (1)

University of Pittsburgh¹

01 Oct 2011-Current Opinion in Immunology (NIH Public Access)-Vol. 23, Iss: 5, pp 613-619

TL;DR: A review of recent advances in the field of IL-17/IL-17 receptor family biology, with an emphasis on IL- 17A biology.

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About: This article is published in Current Opinion in Immunology.The article was published on 2011-10-01 and is currently open access. It has received 258 citations till now. The article focuses on the topics: Janus kinase 1 & Common gamma chain.

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Journal Article•DOI•

Role of cytokines in intervertebral disc degeneration: pain and disc content.

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Makarand V. Risbud, Irving M. Shapiro

01 Jan 2014-Nature Reviews Rheumatology

TL;DR: An enhanced understanding of the contribution of cytokines and immune cells to these catabolic, angiogenic and nociceptive processes could provide new targets for the treatment of symptomatic disc disease.

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Abstract: Degeneration of the intervertebral discs (IVDs) is a major contributor to back, neck and radicular pain. IVD degeneration is characterized by increases in levels of the proinflammatory cytokines TNF, IL-1α, IL-1β, IL-6 and IL-17 secreted by the IVD cells; these cytokines promote extracellular matrix degradation, chemokine production and changes in IVD cell phenotype. The resulting imbalance in catabolic and anabolic responses leads to the degeneration of IVD tissues, as well as disc herniation and radicular pain. The release of chemokines from degenerating discs promotes the infiltration and activation of immune cells, further amplifying the inflammatory cascade. Leukocyte migration into the IVD is accompanied by the appearance of microvasculature tissue and nerve fibres. Furthermore, neurogenic factors, generated by both disc and immune cells, induce expression of pain-associated cation channels in the dorsal root ganglion. Depolarization of these ion channels is likely to promote discogenic and radicular pain, and reinforce the cytokine-mediated degenerative cascade. Taken together, an enhanced understanding of the contribution of cytokines and immune cells to these catabolic, angiogenic and nociceptive processes could provide new targets for the treatment of symptomatic disc disease. In this Review, the role of key inflammatory cytokines during each of the individual phases of degenerative disc disease, as well as the outcomes of major clinical studies aimed at blocking cytokine function, are discussed.

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1,053 citations

Journal Article•DOI•

STAT3 signaling in immunity.

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Emily J. Hillmer¹, Huiyuan Zhang¹, Haiyan S. Li¹, Stephanie S. Watowich², Stephanie S. Watowich¹ - Show less +1 more•Institutions (2)

University of Texas MD Anderson Cancer Center¹, University of Texas at Austin²

01 Oct 2016-Cytokine & Growth Factor Reviews

TL;DR: Information on the numerous and distinct biological actions of STAT3 is summarized, and recent discoveries are highlighted, with a specific focus on STAT3 function in the immune and hematopoietic systems.

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393 citations

Cites background from "Recent advances in the IL-17 cytoki..."

...of immune effectors such as anti-microbial peptides, chemokines and granulopoietic cytokines [208,209]....
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Journal Article•DOI•

The emerging role of IL-17 in the pathogenesis of psoriasis: preclinical and clinical findings.

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David Martin¹, Jennifer E. Towne¹, Gregory Kricorian¹, Paul Klekotka¹, Johann E. Gudjonsson², James G. Krueger³, Chris B. Russell¹ - Show less +3 more•Institutions (3)

Amgen¹, University of Michigan², Rockefeller University³

01 Jan 2013-Journal of Investigative Dermatology

TL;DR: This review focuses on the emerging biology of the IL- 17 cytokine family in psoriasis, and on the molecular and genetic information gained from animal models and human clinical studies that confirm IL-17 as a crucial proinflammatory cytokine in psoriatic lesions.

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390 citations

Cites background from "Recent advances in the IL-17 cytoki..."

...In the TRAF6-independent pathway, Act-1 can bind to TRAF5 and sequester the RNA binding factor SF2, leading to stabilization of inflammatory mRNAs (Hartupee et al., 2007; Gaffen, 2011; Sun et al., 2011; Figure 1)....
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Journal Article•DOI•

TRAF molecules in cell signaling and in human diseases

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Ping Xie¹•Institutions (1)

Rutgers University¹

13 Jun 2013-Journal of Molecular Signaling

TL;DR: An overview of the current knowledge of TRAFs is presented, with an emphasis on recent findings concerning TRAF molecules in signaling and in human diseases.

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Abstract: The tumor necrosis factor receptor (TNF-R)-associated factor (TRAF) family of intracellular proteins were originally identified as signaling adaptors that bind directly to the cytoplasmic regions of receptors of the TNF-R superfamily. The past decade has witnessed rapid expansion of receptor families identified to employ TRAFs for signaling. These include Toll-like receptors (TLRs), NOD-like receptors (NLRs), RIG-I-like receptors (RLRs), T cell receptor, IL-1 receptor family, IL-17 receptors, IFN receptors and TGFβ receptors. In addition to their role as adaptor proteins, most TRAFs also act as E3 ubiquitin ligases to activate downstream signaling events. TRAF-dependent signaling pathways typically lead to the activation of nuclear factor-κBs (NF-κBs), mitogen-activated protein kinases (MAPKs), or interferon-regulatory factors (IRFs). Compelling evidence obtained from germ-line and cell-specific TRAF-deficient mice demonstrates that each TRAF plays indispensable and non-redundant physiological roles, regulating innate and adaptive immunity, embryonic development, tissue homeostasis, stress response, and bone metabolism. Notably, mounting evidence implicates TRAFs in the pathogenesis of human diseases such as cancers and autoimmune diseases, which has sparked new appreciation and interest in TRAF research. This review presents an overview of the current knowledge of TRAFs, with an emphasis on recent findings concerning TRAF molecules in signaling and in human diseases.

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387 citations

Cites background from "Recent advances in the IL-17 cytoki..."

...On the other hand, TRAF6 also induces GSK3β activation likely through PI-3K, and ERK1/2 activation likely through Raf1 [12,151,159]....
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...Activated GSK3β and ERK induce dual phosphorylation of C/EBPβ and thereby inhibit its activity [12,151,160]....
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...Interestingly, TRAF2 and TRAF5 transduce the IL-17 signals to stabilize mRNA transcripts of chemokines (such as CXCL1) and cytokines (such as IL-6) by recruiting the splicing factor SF2 (also known as alternative splicing factor, ASF) into the IL-17R-Act1 signaling complex [151,153,161]....
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...The founding member of this family, IL-17, is the defining cytokine of a new T helper cell population termed “Th17”, which contributes significantly to the pathogenesis of multiple autoimmune and inflammatory diseases [150,151]....
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...The binding of TRAF3 to Chemokines, cytokines, anti-microbial peptides and MMPs NF- B1 I B IKK SF2/ASF NEMO MAPKs c/EBP C/EBP TRAF6 GSK3 IL-17RA IL-17A/F Act1 IL-17RC TRAF3 AAAAAAA Chemokine mRNA stability Raf1 TRAF4 Ubc13 Uev1A AP-1?...
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Journal Article•DOI•

The Immunologic Role of IL-17 in Psoriasis and Psoriatic Arthritis Pathogenesis.

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Andrew Blauvelt, Andrea Chiricozzi¹•Institutions (1)

University of Pisa¹

01 Dec 2018-Clinical Reviews in Allergy & Immunology

TL;DR: The immunologic role of interleukin (IL)-17, the major effector cytokine in the pathogenesis of psoriatic disease, is reviewed, along with the rationale for targeting the IL-17 cytokine family (IL-17A, Il-17F, and IL- 17 receptor A) in the treatment of psoriasis and psoratic arthritis.

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Abstract: Psoriasis is a chronic, immune-mediated, inflammatory disease that is pathogenically driven by proinflammatory cytokines. This article reviews the immunologic role of interleukin (IL)-17, the major effector cytokine in the pathogenesis of psoriatic disease, along with the rationale for targeting the IL-17 cytokine family (IL-17A, IL-17F, and IL-17 receptor A) in the treatment of psoriasis and psoriatic arthritis. Emerging evidence indicates that major sources of IL-17A in patients with psoriatic disease are mast cells, γδ T cells, αβ T cells, and innate lymphoid cells in lesional skin and synovial fluid. Within the skin and joints, IL-17A acts on cellular targets, including keratinocytes, neutrophils, endothelial cells, fibroblasts, osteoclasts, chondrocytes, and osteoblasts, to stimulate production of various antimicrobial peptides, chemokines, and proinflammatory and proliferative cytokines, which, in turn, promote tissue inflammation and bone remodeling. The critical importance of the IL-23/IL-17A axis to the pathogenesis of psoriatic disease has resulted in many new biologic treatments targeting these cytokines. These biologics dramatically improve skin and joint symptoms in patients with moderate-to-severe psoriasis and psoriatic arthritis.

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372 citations

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References

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Journal Article•DOI•

The orphan nuclear receptor RORgammat directs the differentiation program of proinflammatory IL-17+ T helper cells.

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Ivaylo I. Ivanov¹, Brent S. McKenzie², Liang Zhou¹, Carlos E. Tadokoro¹, Alice Lepelley¹, Juan J. Lafaille¹, Daniel J. Cua², Dan R. Littman¹ - Show less +4 more•Institutions (2)

New York University¹, Schering-Plough²

22 Sep 2006-Cell

TL;DR: It is shown that the orphan nuclear receptor RORgammat is the key transcription factor that orchestrates the differentiation of this effector cell lineage of proinflammatory T helper cells and its potential as a therapeutic target in inflammatory diseases is highlighted.

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4,616 citations

Journal Article•DOI•

Interleukin 17–producing CD4 + effector T cells develop via a lineage distinct from the T helper type 1 and 2 lineages

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Laurie E. Harrington¹, Robin D. Hatton¹, Paul R. Mangan¹, Henrietta Turner¹, Theresa L. Murphy², Kenneth M. Murphy², Casey T. Weaver¹ - Show less +3 more•Institutions (2)

University of Alabama at Birmingham¹, Washington University in St. Louis²

02 Oct 2005-Nature Immunology

TL;DR: Findings provide a basis for understanding how inhibition of IFN-γ signaling enhances development of pathogenic TH-17 effector cells that can exacerbate autoimmunity.

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Abstract: CD4(+) T cells producing interleukin 17 (IL-17) are associated with autoimmunity, although the precise mechanisms that control their development are undefined. Here we present data that challenge the idea of a shared developmental pathway with T helper type 1 (T(H)1) or T(H)2 lineages and instead favor the idea of a distinct effector lineage we call 'T(H)-17'. The development of T(H)-17 cells from naive precursor cells was potently inhibited by interferon-gamma (IFN-gamma) and IL-4, whereas committed T(H)-17 cells were resistant to suppression by T(H)1 or T(H)2 cytokines. In the absence of IFN-gamma and IL-4, IL-23 induced naive precursor cells to differentiate into T(H)-17 cells independently of the transcription factors STAT1, T-bet, STAT4 and STAT6. These findings provide a basis for understanding how inhibition of IFN-gamma signaling enhances development of pathogenic T(H)-17 effector cells that can exacerbate autoimmunity.

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4,616 citations

"Recent advances in the IL-17 cytoki..." refers background in this paper

...However, they exhibit potent synergy, not only with TNFa but also with LTa, IFNg and IL-1b [4,73]....
[...]
...These 3 articles show that Th17/IL-17 responses can induce Th1/IFNg responses in the context of intracellular infections....
[...]
...Although Th1 cells can suppress Th17 generation via inhibitory signals from IFNg [19,20], IL-17 can positively regulate Th1 cell differentiation in certain intracellular infections or vaccination settings, including M. tuberculosis, Francisella tularensis and chlamydial infections [21 ,22 ,23 ]....
[...]
...Although Th1 cells can suppress Th17 generation via inhibitory signals from IFNg [19,20], IL-17 can positively regulate Th1 cell differentiation in certain intracellular infections or vaccination settings, including M....
[...]
...Interconnections among T cell subsets Although Th17 cells are often depicted as a committed lineage, in fact there are many interrelationships with other subpopulations, including functional cooperation, cells that express signature cytokines from multiple subsets (e.g. IL-17 + IFNg+ cells) and lineage plasticity....
[...]

Journal Article•DOI•

A distinct lineage of CD4 T cells regulates tissue inflammation by producing interleukin 17

[...]

Heon Park¹, Zhaoxia Li¹, Xuexian O. Yang², Seon Hee Chang, Roza Nurieva, Yi Hong Wang², Ying Wang¹, Leroy Hood³, Zhou Zhu⁴, Qiang Tian³, Chen Dong² - Show less +7 more•Institutions (4)

University of Washington¹, University of Texas MD Anderson Cancer Center², Institute for Systems Biology³, Johns Hopkins University⁴

01 Nov 2005-Nature Immunology

TL;DR: In vivo, antibody to IL- 17 inhibited chemokine expression in the brain during experimental autoimmune encephalomyelitis, whereas overexpression of IL-17 in lung epithelium caused Chemokine production and leukocyte infiltration, indicating a unique T helper lineage that regulates tissue inflammation.

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Abstract: Interleukin 17 (IL-17) has been linked to autoimmune diseases, although its regulation and function have remained unclear. Here we have evaluated in vitro and in vivo the requirements for the differentiation of naive CD4 T cells into effector T helper cells that produce IL-17. This process required the costimulatory molecules CD28 and ICOS but was independent of the cytokines and transcription factors required for T helper type 1 or type 2 differentiation. Furthermore, both IL-4 and interferon-γ negatively regulated T helper cell production of IL-17 in the effector phase. In vivo, antibody to IL-17 inhibited chemokine expression in the brain during experimental autoimmune encephalomyelitis, whereas overexpression of IL-17 in lung epithelium caused chemokine production and leukocyte infiltration. Thus, IL-17 expression characterizes a unique T helper lineage that regulates tissue inflammation.

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4,196 citations

"Recent advances in the IL-17 cytoki..." refers background in this paper

...However, they exhibit potent synergy, not only with TNFa but also with LTa, IFNg and IL-1b [4,73]....
[...]
...These 3 articles show that Th17/IL-17 responses can induce Th1/IFNg responses in the context of intracellular infections....
[...]
...Although Th1 cells can suppress Th17 generation via inhibitory signals from IFNg [19,20], IL-17 can positively regulate Th1 cell differentiation in certain intracellular infections or vaccination settings, including M. tuberculosis, Francisella tularensis and chlamydial infections [21 ,22 ,23 ]....
[...]
...Although Th1 cells can suppress Th17 generation via inhibitory signals from IFNg [19,20], IL-17 can positively regulate Th1 cell differentiation in certain intracellular infections or vaccination settings, including M....
[...]
...Interconnections among T cell subsets Although Th17 cells are often depicted as a committed lineage, in fact there are many interrelationships with other subpopulations, including functional cooperation, cells that express signature cytokines from multiple subsets (e.g. IL-17 + IFNg+ cells) and lineage plasticity....
[...]

Journal Article•DOI•

A Genome-Wide Association Study Identifies IL23R as an Inflammatory Bowel Disease Gene

[...]

Richard H. Duerr¹, Kent D. Taylor², Steven R. Brant³, Steven R. Brant⁴, John D. Rioux⁵, John D. Rioux⁶, Mark S. Silverberg⁷, Mark J. Daly⁶, Mark J. Daly⁸, A. Hillary Steinhart⁷, Clara Abraham⁹, Miguel Regueiro¹, Anne M. Griffiths⁷, Themistocles Dassopoulos³, Alain Bitton¹⁰, Huiying Yang², Stephan R. Targan², Lisa W. Datta⁴, Emily O. Kistner⁹, L. Philip Schumm⁹, Annette Lee¹¹, Peter K. Gregersen¹¹, M. Michael Barmada¹, Jerome I. Rotter², Dan L. Nicolae⁹, Judy H. Cho¹² - Show less +22 more•Institutions (12)

University of Pittsburgh¹, Cedars-Sinai Medical Center², Johns Hopkins University³, Johns Hopkins University School of Medicine⁴, Université de Montréal⁵, Broad Institute⁶, University of Toronto⁷, Harvard University⁸, University of Chicago⁹, McGill University¹⁰, North Shore-LIJ Health System¹¹, Yale University¹²

01 Dec 2006-Science

TL;DR: A highly significant association is found between Crohn's disease and the IL23R gene on chromosome 1p31, which encodes a subunit of the receptor for the proinflammatory cytokine interleukin-23, which prioritize this signaling pathway as a therapeutic target in inflammatory bowel disease.

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Abstract: The inflammatory bowel diseases Crohn's disease and ulcerative colitis are common, chronic disorders that cause abdominal pain, diarrhea, and gastrointestinal bleeding. To identify genetic factors that might contribute to these disorders, we performed a genome-wide association study. We found a highly significant association between Crohn's disease and the IL23R gene on chromosome 1p31, which encodes a subunit of the receptor for the proinflammatory cytokine interleukin-23. An uncommon coding variant (rs11209026, c.1142G>A, p.Arg381Gln) confers strong protection against Crohn's disease, and additional noncoding IL23R variants are independently associated. Replication studies confirmed IL23R associations in independent cohorts of patients with Crohn's disease or ulcerative colitis. These results and previous studies on the proinflammatory role of IL-23 prioritize this signaling pathway as a therapeutic target in inflammatory bowel disease.

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2,937 citations

Journal Article•DOI•

Divergent Pro- and Antiinflammatory Roles for IL-23 and IL-12 in Joint Autoimmune Inflammation

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Craig A. Murphy, Claire L. Langrish, Yi Yi Chen, Wendy M. Blumenschein, Terrill K. McClanahan, Robert A. Kastelein, Jonathon D. Sedgwick, Daniel J. Cua - Show less +4 more

15 Dec 2003-Journal of Experimental Medicine

TL;DR: The data presented here indicate that IL-23 is an essential promoter of end-stage joint autoimmune inflammation, whereas IL-12 paradoxically mediates protection from autoimmune inflammation.

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Abstract: Interleukin (IL) 23 is a heterodimeric cytokine composed of a p19 subunit and the p40 subunit of IL-12. IL-23 affects memory T cell and inflammatory macrophage function through engagement of a novel receptor (IL-23R) on these cells. Recent analysis of the contribution of IL-12 and IL-23 to central nervous system autoimmune inflammation demonstrated that IL-23 rather than IL-12 was the essential cytokine. Using gene-targeted mice lacking only IL-12 (p35−/−) or IL-23 (p19−/−), we show that the specific absence of IL-23 is protective, whereas loss of IL-12 exacerbates collagen-induced arthritis. IL-23 gene-targeted mice did not develop clinical signs of disease and were completely resistant to the development of joint and bone pathology. Resistance correlated with an absence of IL-17–producing CD4+ T cells despite normal induction of collagen-specific, interferon-γ–producing T helper 1 cells. In contrast, IL-12–deficient p35−/− mice developed more IL-17–producing CD4+ T cells, as well as elevated mRNA expression of proinflammatory tumor necrosis factor, IL-1β, IL-6, and IL-17 in affected tissues of diseased mice. The data presented here indicate that IL-23 is an essential promoter of end-stage joint autoimmune inflammation, whereas IL-12 paradoxically mediates protection from autoimmune inflammation.

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1,695 citations