Interleukins are a vital part of the pathway that regulates inflammation in the body. There are many different types of interleukins.
Interleukins play a key role in the development or progression of inflammatory conditions.
Inflammation and Interleukins. Inflammation (Latin, inflammatio, to set on fire) is the complex biological response of vascular tissues to harmful stimuli, such as pathogens, damaged cells, or irritants. It is a protective attempt by the organism to remove the injurious stimuli as well as initiate the healing process for the tissue. Inflammation is not a synonym for infection. Wikipedia.
Soluble TNF-R1, VEGF and other cytokines as markers of disease activity in systemic lupus erythematosus (SLE) and lupus nephritis (LN). These results indicate that for active LN, sTNF-R1 could be a useful serum cytokine marker, with potential for vascular endothelial growth factor in the urine. PubMed, Lupus, 2019 May 2:961203319845487. (Also see Diagnosis of Lupus)
Y-27632, a Rho–associated protein kinase inhibitor, inhibits systemic lupus erythematosus. The findings showed that the inhibition of rho-associated, coiled–coil–containing protein kinase 1(ROCK) was beneficial for the prevention of systemic lupus erythematosus, which possibly by suppressing NF-κB activation. PubMed, Biomed Pharmacother, 2017 Apr;88:359-366. (Also see Research on Systemic Lupus Erythematosus)
Cantargia Selects CAN10 as Development Project in Systemic Sclerosis and Myocarditis. Cantargia develops antibody-based pharmaceuticals against the interleukin 1 receptor accessory protein (IL1RAP) and the project will focus on unmet medical need in systemic sclerosis and myocarditis. PR Newswire, 12/05/2019.
The Roles of IL-1 Family Cytokines in the Pathogenesis of Systemic Sclerosis (SSc). Here, we aim to give a brief overview of IL-1 family cytokines and discuss their pivotal roles in the pathogenesis of SSc. PubMed, Front Immunol, 2019 Sep 13;10:2025.
The IL-1 family of cytokines. Do they have a role in scleroderma fibrosis? Recent analyses of the IL-1 family of cytokines have demonstrated that many of them play a role in skin inflammation and fibrosis and their corresponding antagonists (IL-1RA and IL-36RA) can abrogate this pathology. PubMed, Immunol Lett, 12/04/2017.
Association of interleukin-1 family cytokines single nucleotide polymorphisms with susceptibility to systemic sclerosis: an independent case-control study and a meta-analysis. Results showed that IL-1A -889C/T (rs1800587) was associated with SSc susceptibility in the Chinese population. PubMed, Immunol Res, 2016 Aug;64(4):1041-52.
Therapeutic interleukin-6 blockade reverses transforming growth factor-beta pathway activation in dermal fibroblasts: insights from the faSScinate clinical trial in systemic sclerosis (SSc). The profound impact of IL-6R blockade on the activated fibroblast phenotype highlights the potential of IL-6 as a therapeutic target in SSc and other fibrotic diseases. PubMed, Ann Rheum Dis, 05/31/2018. (Also see Clinical Trials)
The combination of IL-6 and its soluble receptor is associated with the response of rheumatoid arthritis (RA) patients to tocilizumab. RA patients could be easily stratified prior to therapeutic intervention with two molecules related to the pathway blocked by tocilizumab. Seminars in Arthritis and Rheumatism, 11/03/2017. (Also see Treatments for Rheumatoid Arthritis)
The role and therapeutic targeting of IL-6 in rheumatoid arthritis (RA). The prospects for future applications, new therapeutic strategies of IL-6 targeting therapy and relevant issues with regard to the clinical management of IL-6 blockade in RA are discussed. PubMed, Expert Rev Clin Immunol, 2017 Jun;13(6):535-551. (Also see Causes of Rheumatoid Arthritis)
Scleroderma (SSc) peripheral B lymphocytes secrete interleukin-6 and TGF–ß and activate fibroblasts. Peripheral B lymphocytes from SSc patients secreted IL-6 and TGF–ß, and activated fibroblasts in vitro. PubMed, Arthritis Rheumatol, 12/19/2016. (Also see Fibroblasts)
Mechanistic insight into the norepinephrine (NE)–induced fibrosis in systemic sclerosis (SSc). These results suggest that cold exposure and/or emotional stress–induced NE might contribute to the skin fibrosis via potentiation of IL-6 production from fibroblasts in SSc. PMC, Sci Rep, 2016; 6: 34012.(Also see Fibroblasts)
IL-8 and IL-6 primarily mediate the inflammatory response in fibromyalgia (FM) patients. These findings indicate that IL-6 and IL-8 are two of the most constant inflammatory mediators in FM and that their levels correlate significantly with the severity of symptoms. PubMed, J Neuroimmunol, 2016 Jan 15;290:22-5.
Elevated α-defensin levels in plasma and bronchoalveolar lavage fluid from patients with myositis-associated interstitial lung disease. Further studies are necessary to clarify whether human neutrophil peptides represent disease markers and play roles in disease pathogenesis. PubMed, BMC Pulm Med, 2018 Mar 12;18(1):44.
Interleukin-10 gene promoter and Nuclear factor-kB (NFKB)1 promoter insertion/deletion polymorphisms in systemic sclerosis (SSc). The association of the high-producing phenotype (GCC(+) /GCC(+) ) with increased risk for SSc was confirmed, but found no correlation with NFKB polymorphisms. PubMed, Scand J Immunol.
Influence of tyrosine kinase 2 (TYK2) in systemic sclerosis (SSc) susceptibility: a new locus in the IL-12 pathway. The association of TYK2 with SSc and reinforcing the relevance of the IL-12 pathway in SSc pathophysiology is reported for the first time. PubMed, Ann Rheum Dis, 2016 Aug;75(8):1521-6.
Association of interleukin 13 gene polymorphisms and plasma IL 13 level with risk of systemic lupus erythematosus (SLE). The concentration of IL-13 was significantly elevated in rs20541 CT/TT genotypes compared with CC genotype which suggests that rs20541 CT/TT genotypes may be a risk factor for SLE. PubMed, Cytokine, 10/07/2017. (Also see Causes of Lupus)
Transforming growth factor-ß increases interleukin-13 synthesis via GATA-3 transcription factor in T-lymphocytes from patients with systemic sclerosis (SSc). These results demonstrate that TGF-ß upregulates IL-13 synthesis through GATA-3 expression in the T lymphocytes of patients with SSc, confirming that the GATA-3 transcription factor can be regarded as a novel therapeutic target in patients with SSc. PubMed, Arthritis Res Ther. (Also see Molecular Defect)
Role of interleukin-13 in fibrosis, particularly systemic sclerosis. This review examines the role of IL-13 in driving fibrosis with a particular emphasis on systemic sclerosis as a prototypical fibrotic disease. PubMed, Biofactors.
IL-16 expression is increased in the skin and sera of patients with systemic sclerosis. The regional up-regulation of IL-16 in the skin is not only associated with skin sclerosis, but also with systemic IL-16 activation. PubMed, Rheumatology (Oxford), 08/03/2019. (Also see Skin Fibrosis)
Serum concentrations of IL-17A, IL-17B, IL-17E and IL-17F in patients with systemic sclerosis (SSc). Increased synthesis of IL-17B, IL-17E and IL-17F appears to play a role in the pathogenesis of SSc, in contrast to IL-17A. PubMed, Arch Med Sci, 2019 May;15(3):706-712.
Interleukin-17 pathways in systemic sclerosis–associated fibrosis. There is multitude of evidence from across different tissues that interleukin-17 (IL-17) and its downstream pathways are strongly associated with the initiation and propagation of fibrosis. PubMed, Rheumatol Int, 05/09/2019. (Also see Skin Fibrosis)
Expression of interleukin-17 in primary Sjögren's syndrome (pSS) and the correlation with disease severity: A systematic review and meta–analysis. The expression of IL-17 is obviously increased in patients with pSS, especially among those without immunosuppressive treatment. PubMed, Scand J Immunol, 2018 Apr;87(4):e12649. (Also see Sjögren's Syndrome Research)
IL-10-producing regulatory B cells (B10 cells), IL-17+ T cells and autoantibodies in systemic sclerosis. in SSc, B10 cells did not correlate with SSc-specific autoAbs and exhibited an inverse correlation with IL-17+ T cells and IFN?+ T cells. PubMed, Clin Immunol, 2017 Nov;184:26-32.
Th-17 cytokines and interstitial lung involvement in systemic sclerosis. in diffuse SSc patients our results show a clear link between Th-17 cytokines measured both in EBC and in serum with interstitial lung involvement. PubMed, J Breath Res, 2016 Nov 21;10(4):046013.
Serum 25–OH vitamin D level in treatment–naïve systemic lupus erythematosus (SLE) patients: Relation to disease activity, IL-23 and IL-17. Hypovitaminosis D contributes to ANA antibody production and is associated with high serum levels of IL-23 and IL-17 and may trigger the inflammatory process in SLE. Lupus, 12/07/2016. (Also see Research on Systemic Lupus Erythematosus)
Serum level of interleukin-17A in patients with alopecia areata (AA) and its relationship to age. It is possible that IL-17A plays a role in the pathogenesis of AA. Serum IL-17A may be influenced by patient age and age of onset of AA but does not seem to influence disease severity. PubMed, Int J Dermatol. (Also see Alopecia)
Expression of interleukin-18 in muscle tissue of patients with polymyositis or dermatomyositis and effects of conventional immunosuppressive treatment. IL-18 is highly expressed in muscle tissue in the context of inflammatory myopathies and based on its plausible effector functions could provide a novel therapeutic target in future. PubMed, Rheumatology (Oxford), 08/08/2018. (Also see Treatments for Dermatomyositis and Polymyositis)
Interleukin-20 is triggered by toll–like receptor ligands (TLR) and associates with disease activity in patients with rheumatoid arthritis (RA). Our data showed that IL-20 is independently associated with RA disease activity and may be triggered by TLR ligands at local sites of inflammation. PubMed, Cytokine, 2017 Sep;97:187-192. (Also see Causes of Rheumatoid Arthritis)
Autoantibodies (AAbs) against interleukin-21 correlate with disease activity in patients with rheumatoid arthritis (RA). The levels of AAbs against IL-21 correlate with disease activity, which suggests that anti–IL-21 AAbs may play a role in the pathogenesis of RA. PubMed, Clin Rheumatol, 10/10/2017. (Also see Causes of Rheumatoid Arthritis)
IL-22 capacitates dermal fibroblast responses to tumour necrosis factor (TNF) in scleroderma. IL-22 capacitates fibroblast responses to TNF and promotes a proinflammatory fibroblast phenotype by favouring TNF-induced keratinocyte activation. PubMed, Ann Rheum Dis, 2016 Sep;75(9):1697-705.
Dysregulated interleukin-23 signalling contributes to the increased collagen production in scleroderma fibroblasts via balancing microRNA expression. Clarification of the regulatory mechanism of tissue fibrosis by IL-23 in SSc skin may lead to a better understanding of this disease and new therapeutic approaches. PubMed, Rheumatology (Oxford), 2017 Jan;56(1):145-155.
Pivotal Roles of T-Helper 17-Related Cytokines, IL-17, IL-22, and IL-23, in Inflammatory Diseases. Although some conflicting findings still need to be resolved, targeting Th17 cells and their related cytokines such as IL-17, IL-22, and IL-23 may be an effective therapeutic approach for chronic inflammation in the future. Clinical and Developmental Immunology.
IL-25 blockade inhibits metastasis in breast cancer. Inhibition of IL-25 resulted in decreased type 2 T cells and macrophages in the primary tumor microenvironments, both reported to enhance breast tumor invasion and subsequent metastasis to the lung. PubMed, Protein Cell, 2017 Mar;8(3):191-201. (Also see Cancer)
IL-26 Plays Antimicrobial Role in Immune Response. Interleukin 17-producing helper T cells (Th17 cells) secrete copious amounts of interleukin 26 (IL-26) in patients with such autoimmune diseases as rheumatoid arthritis, psoriasis and inflammatory bowel disease. The Rheumatologist.
The IL-33 gene is related to increased susceptibility to systemic sclerosis (SSc). The aim of the present study was to detect the potential association of IL-33 gene polymorphisms on the susceptibility of SSc. Springer Link 01/07/2016.
We have the world's best supporters! See ISN News.
SCLERO.ORG is the world's leading nonprofit for trustworthy research, support, education and awareness for scleroderma and related illnesses. We are a 501(c)(3) U.S.-based public charitable foundation, established in 2002. Meet Our Team. Donations may also be mailed to: